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Tymko MM, Drapeau A, Vieira-Coelho MA, Labrecque L, Imhoff S, Coombs GB, Langevin S, Fortin M, Châteauvert N, Ainslie PN, Brassard P. New evidence for baroreflex and respiratory chemoreflex-mediated cerebral sympathetic activation in humans. J Appl Physiol (1985) 2025; 138:366-377. [PMID: 39718204 DOI: 10.1152/japplphysiol.00688.2024] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/10/2024] [Revised: 12/12/2024] [Accepted: 12/13/2024] [Indexed: 12/25/2024] Open
Abstract
The brain is highly innervated by sympathetic nerve fibers; however, their physiological purpose is poorly understood. We hypothesized that unilateral cerebral norepinephrine (NE) spillover, an index of cerebral sympathetic nerve activity (SNA), would be elevated when engaging the baroreflex [via lower-body negative pressure (LBNP; -20 and -40 Torr)] and respiratory chemoreflexes [via carbon dioxide (CO2) administration (+8 Torr)], independently and in combination. Twelve young and healthy participants (five females) underwent simultaneous blood sampling from the right radial artery and internal jugular vein. Tritiated NE was infused through the participants' right forearm vein. Right internal jugular vein and internal carotid artery blood flow were measured using duplex ultrasound. Unilateral cerebral NE spillover remained unchanged when only LBNP was applied (P = 0.29) but increased with hypercapnia (P = 0.035) and -40 Torr LBNP + CO2 (P < 0.01). There were no changes in total NE spillover during the LBNP and LBNP + CO2 trials (both P = 0.66), nor during CO2 alone (P = 0.13). No correlations were present between the increase in unilateral cerebral NE spillover during -40 Torr LBNP + CO2 and reductions in internal carotid artery blood flow (P = 0.56). These results indicate that baroreflex and respiratory chemoreflex stressors elevate cerebral SNA; however, the observed cerebral sympathetic activation has no impact on blood flow regulation in the internal carotid artery.NEW & NOTEWORTHY The results of the current study suggest that baroreflex and respiratory chemoreflex stressors elevate cerebral sympathetic nervous activity, quantified using the brain norepinephrine spillover method. However, the observed cerebral sympathetic activation has no impact on blood flow regulation in the internal carotid artery.
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Affiliation(s)
- Michael M Tymko
- Integrative Cerebrovascular and Environmental Physiology SB Laboratory, Department of Human Health and Nutritional Sciences, College of Biological Science, University of Guelph, Guelph, Ontario, Canada
- Department of Medicine, Faculty of Medicine, University of British Columbia, Vancouver, British Columbia, Canada
| | - Audrey Drapeau
- Department of Kinesiology, Faculty of Medicine, Université Laval, Québec, Québec, Canada
- Institut universitaire de cardiologie et de pneumologie de Québec, Université Laval, Québec, Canada
| | - Maria Augusta Vieira-Coelho
- Pharmacology and Therapeutics Unit, Faculty of Medicine, Department of Biomedicine, University of Porto, Porto, Portugal
- Department of Psychiatry and Mental Health, University Hospital Center of São João, Porto, Portugal
| | - Lawrence Labrecque
- Department of Kinesiology, Faculty of Medicine, Université Laval, Québec, Québec, Canada
- Institut universitaire de cardiologie et de pneumologie de Québec, Université Laval, Québec, Canada
| | - Sarah Imhoff
- Department of Kinesiology, Faculty of Medicine, Université Laval, Québec, Québec, Canada
- Institut universitaire de cardiologie et de pneumologie de Québec, Université Laval, Québec, Canada
| | - Geoff B Coombs
- School of Psychology and Sport Science, Bangor University, Wales, United Kingdom
| | - Stephan Langevin
- Institut universitaire de cardiologie et de pneumologie de Québec, Université Laval, Québec, Canada
| | - Marc Fortin
- Institut universitaire de cardiologie et de pneumologie de Québec, Université Laval, Québec, Canada
| | - Nathalie Châteauvert
- Institut universitaire de cardiologie et de pneumologie de Québec, Université Laval, Québec, Canada
| | - Philip N Ainslie
- Centre for Heart, Lung and Vascular Health, School of Health and Exercise Sciences, University of British Columbia - Okanagan, Kelowna, British Columbia, Canada
| | - Patrice Brassard
- Department of Kinesiology, Faculty of Medicine, Université Laval, Québec, Québec, Canada
- Institut universitaire de cardiologie et de pneumologie de Québec, Université Laval, Québec, Canada
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2
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Cui HC, Chang ZQ, Zhao SK. Atypical cervical spondylotic radiculopathy resulting in a hypertensive emergency during cervical extension: A case report and review of literature. World J Orthop 2024; 15:981-990. [DOI: 10.5312/wjo.v15.i10.981] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/16/2024] [Revised: 09/06/2024] [Accepted: 09/14/2024] [Indexed: 10/11/2024] Open
Abstract
BACKGROUND Extensive research revealed the absence of reports documenting hypertensive emergencies precipitated by changes in the cervical spine posture.
CASE SUMMARY We here present a 57-year-old woman diagnosed as having cervical spondylotic radiculopathy (CSR) who was scheduled for anterior cervical decompression and fusion. During post-anesthetic positioning, a sudden hypertensive surge was observed when the patient was in a supine position with the neck being slightly extended. This surge was promptly reversed through cervical flexion and head elevation. This event however required an alternate surgical approach for recovery—posterior laminoplasty and endoscopy-assisted nucleus pulposus removal. Following the 6-month outpatient follow-up period, cervical flexion and extension activities substantially improved in the patient without any episodes of increase in acute blood pressure.
CONCLUSION Maintaining a safe hypotensive posture and performing rapid, thorough decompression surgery may serve as effective interventions for patients presenting symptoms similar to those of CSR accompanied by hypertensive emergencies (HE). This would mitigate the underlying causes of these HEs.
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Affiliation(s)
- Hao-Cheng Cui
- Department of Orthopedic Surgery, 960th Hospital of PLA, Jinan 250031, Shandong Province, China
| | - Zheng-Qi Chang
- Department of Orthopedic Surgery, 960th Hospital of PLA, Jinan 250031, Shandong Province, China
| | - Shao-Ke Zhao
- Department of Orthopedic Surgery, 960th Hospital of PLA, Jinan 250031, Shandong Province, China
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Takara S, Kida H, Inoue T. Development of implantable devices for epilepsy: research with cats, dogs, and macaques in biomedical engineering. Adv Robot 2024; 38:983-1007. [DOI: 10.1080/01691864.2024.2345655] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/13/2023] [Revised: 02/22/2024] [Accepted: 03/20/2024] [Indexed: 01/06/2025]
Affiliation(s)
- Sayuki Takara
- Research Center for Advanced Science and Innovation, Organization for Research Initiatives, Yamaguchi University, Ube, Japan
| | - Hiroyuki Kida
- Department of Physiology, Yamaguchi University Graduate School of Medicine, Ube, Japan
| | - Takao Inoue
- Research Center for Advanced Science and Innovation, Organization for Research Initiatives, Yamaguchi University, Ube, Japan
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Matsuo N, Matsuo S, Nakamura Y, Ezomo FO, Kawai Y. Regulatory effects of cervical sympathetic trunk and renal sympathetic nerve activities on cerebral blood flow during head-down postural rotations. Auton Neurosci 2020; 229:102738. [PMID: 33197695 DOI: 10.1016/j.autneu.2020.102738] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/12/2020] [Revised: 10/28/2020] [Accepted: 10/29/2020] [Indexed: 11/19/2022]
Abstract
This study attempts to clarify the neural control of cerebral blood flow (CBF) during head-down postural rotation, which induces a cephalad fluid shift in urethane-anesthetized rats. The animals were placed on a table, tilted to a 45° head-down position over 5 s and maintained in that position. Head-down rotation (HDR) induced a transient decrease (8 ± 3 mm Hg; mean ± SE) in mean arterial blood pressure (ABP) at 7.3 ± 0.3 s after the onset of HDR. The pressure returned to the pre-HDR level within 1 min in the head-down position. Pretreatment with hexamethonium bromide suppressed the HDR-elicited decrease in ABP, suggesting that the decrease in ABP was induced by the suppression of autonomic neural outflow. The administration of phenoxybenzamine (PB), an α-adrenergic antagonist, also eliminated the HDR-elicited decrease in ABP, suggesting that this decrease was elicited by the suppression of α-adrenergic vascular tone. To test sympathetic outflow during HDR, renal sympathetic nerve activity (RSNA) and cervical sympathetic trunk (CST) activity (CSTA) were recorded. RSNA was transiently suppressed at 2.3 ± 0.4 s after HDR onset, followed by a decrease in ABP, suggesting that this decrease was, at least in part, induced by the suppression of sympathetic nerves. CSTA did not change significantly during HDR. These results suggest that HDR suppresses sympathetic nerves in the lower body rather than in the head, which might result in a decrease in ABP. To test the effect of the decrease in ABP due to sympathetic activity on CBF during HDR, changes in CBF during HDR were measured. CBF did not change significantly during HDR in the control group after the administration of an α-receptor blocker or after denervation of the CSTs. These results suggest that the impact of the CSTs on CBF is likely to be limited by a rapid increase in CBF due to HDR-elicited cephalad fluid shift and that CBF autoregulation proceeds through an alternative mechanism involving the myogenic properties of cerebral vessels.
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Affiliation(s)
- Noriko Matsuo
- Division of Adaptation Physiology, Department of Physiology, Tottori University Faculty of Medicine, 86 Nishi-cho, Yonago 683-8503, Japan
| | - Satoshi Matsuo
- Division of Adaptation Physiology, Department of Physiology, Tottori University Faculty of Medicine, 86 Nishi-cho, Yonago 683-8503, Japan.
| | - Yosuke Nakamura
- Division of Adaptation Physiology, Department of Physiology, Tottori University Faculty of Medicine, 86 Nishi-cho, Yonago 683-8503, Japan
| | - Felix Ojeiru Ezomo
- Division of Adaptation Physiology, Department of Physiology, Tottori University Faculty of Medicine, 86 Nishi-cho, Yonago 683-8503, Japan
| | - Yasuaki Kawai
- Division of Adaptation Physiology, Department of Physiology, Tottori University Faculty of Medicine, 86 Nishi-cho, Yonago 683-8503, Japan
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Fenrich M, Habjanovic K, Kajan J, Heffer M. The circle of Willis revisited: Forebrain dehydration sensing facilitated by the anterior communicating artery: How hemodynamic properties facilitate more efficient dehydration sensing in amniotes. Bioessays 2020; 43:e2000115. [PMID: 33191609 DOI: 10.1002/bies.202000115] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Key Words] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/13/2020] [Revised: 10/10/2020] [Accepted: 10/13/2020] [Indexed: 12/14/2022]
Abstract
We hypothesize that threat of dehydration provided selection pressure for the evolutionary emergence and persistence of the anterior communicating artery (ACoA - the inter-arterial connection that completes the Circle of Willis) in early amniotes. The ACoA is a hemodynamically insignificant artery, but, as we argue in this paper, its privileged position outside the blood-brain barrier gives it a crucial sensing function for the osmolarity of the blood against the background of the rest of the brain, which efficiently protects itself from dehydration. Till now, the questions of why the ACoA evolved, and what its physiological function is, have remained unsatisfactorily answered. The traditional view-that the ACoA serves as a collateral source of vascularization in case of arterial stenosis-is anthropocentric, and not in accordance with principles of natural selection that apply more generally. Diseases underlying arterial stenosis are associated with aging and the human lifestyle, so this cannot explain why the ACoA formed hundreds of millions of years ago and persisted in amniotes to this day. The peculiar hemodynamic properties of the ACoA could be selected traits that allowed for more efficient forebrain detection of dehydration and complex behavioral responses to water loss, a major advantage in the survival of early amniotes. This hypothesis also explains insufficient hydration often seen in elderly humans.
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Affiliation(s)
- Matija Fenrich
- Laboratory of Neurobiology, Faculty of Medicine, J. J. Strossmayer University of Osijek, Osijek, Croatia
| | - Karlo Habjanovic
- Laboratory of Neurobiology, Faculty of Medicine, J. J. Strossmayer University of Osijek, Osijek, Croatia
| | - Josip Kajan
- Laboratory of Neurobiology, Faculty of Medicine, J. J. Strossmayer University of Osijek, Osijek, Croatia
| | - Marija Heffer
- Laboratory of Neurobiology, Faculty of Medicine, J. J. Strossmayer University of Osijek, Osijek, Croatia
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Samora M, Vianna LC, Carmo JC, Macedo V, Dawes M, Phillips AA, Paton JFR, Fisher JP. Neurovascular coupling is not influenced by lower body negative pressure in humans. Am J Physiol Heart Circ Physiol 2020; 319:H22-H31. [PMID: 32442032 DOI: 10.1152/ajpheart.00076.2020] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/22/2022]
Abstract
Cerebral blood flow is tightly coupled with local neuronal activation and metabolism, i.e., neurovascular coupling (NVC). Studies suggest a role of sympathetic nervous system in the regulation of cerebral blood flow. However, this is controversial, and the sympathetic regulation of NVC in humans remains unclear. Since impaired NVC has been identified in several chronic diseases associated with a heightened sympathetic activity, we aimed to determine whether reflex-mediated sympathetic activation via lower body negative pressure (LBNP) attenuates NVC in humans. NVC was assessed using a visual stimulation protocol (5 cycles of 30 s eyes closed and 30 s of reading) in 11 healthy participants (aged 24 ± 3 yr). NVC assessments were made under control conditions and during LBNP at -20 and -40 mmHg. Posterior (PCA) and middle (MCA) cerebral artery mean blood velocity (Vmean) and vertebral artery blood flow (VAflow) were simultaneously determined with cardiorespiratory variables. Under control conditions, the visual stimulation evoked a robust increase in PCAVmean (∆18.0 ± 4.5%), a moderate rise in VAflow (∆9.6 ± 4.3%), and a modest increase in MCAVmean (∆3.0 ± 1.9%). The magnitude of NVC response was not affected by mild-to-moderate LBNP (all P > 0.05 for repeated-measures ANOVA). Given the small change that occurred in partial pressure of end-tidal CO2 during LBNP, this hypocapnia condition was matched via voluntary hyperventilation in absence of LBNP in a subgroup of participants (n = 8). The mild hypocapnia during LBNP did not exert a confounding influence on the NVC response. These findings indicate that the NVC is not influenced by LBNP or mild hypocapnia in humans.NEW & NOTEWORTHY Visual stimulation evoked a robust increase in posterior cerebral artery velocity and a modest increase in vertebral artery blood flow, i.e., neurovascular coupling (NVC), which was unaffected by lower body negative pressure (LBNP) in humans. In addition, although LBNP induced a mild hypocapnia, this degree of hypocapnia in the absence of LBNP failed to modify the NVC response.
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Affiliation(s)
- Milena Samora
- Department of Physiology, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand.,NeuroV̇ASQ̇-Integrative Physiology Laboratory, Faculty of Physical Education, University of Brasília, Brasília, Distrito Federal, Brazil
| | - Lauro C Vianna
- NeuroV̇ASQ̇-Integrative Physiology Laboratory, Faculty of Physical Education, University of Brasília, Brasília, Distrito Federal, Brazil
| | - Jake C Carmo
- Biomechanics and Biological Signal Processing Laboratory, Faculty of Physical Education, University of Brasília, Brasília, Distrito Federal, Brazil
| | - Victor Macedo
- Biomechanics and Biological Signal Processing Laboratory, Faculty of Physical Education, University of Brasília, Brasília, Distrito Federal, Brazil
| | - Matthew Dawes
- Department of Physiology, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand
| | - Aaron A Phillips
- Departments of Physiology, Pharmacology, and Clinical Neurosciences, Libin Cardiovascular Institute, Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Alberta, Canada
| | - Julian F R Paton
- Department of Physiology, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand
| | - James P Fisher
- Department of Physiology, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand
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Washio T, Watanabe H, Ogoh S. Dynamic cerebral autoregulation in anterior and posterior cerebral circulation during cold pressor test. J Physiol Sci 2020; 70:1. [PMID: 32039699 PMCID: PMC6987085 DOI: 10.1186/s12576-020-00732-7] [Citation(s) in RCA: 25] [Impact Index Per Article: 5.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/21/2019] [Accepted: 01/22/2020] [Indexed: 12/26/2022]
Abstract
We hypothesized that cerebral blood flow (CBF) regulation in the posterior circulation differs from that of the anterior circulation during a cold pressor test (CPT) and is accompanied by elevations in arterial blood pressure (ABP) and sympathetic nervous activity (SNA). To test this, dynamic cerebral autoregulation (dCA) in the middle and posterior cerebral arteries (MCA and PCA) were measured at three different conditions: control, early phase of the CPT, and the late phase of the CPT. The dCA was examined using a thigh cuff occlusion and release technique. The MCA and PCA blood velocities were unchanged at CPT compared with the control conditions despite an elevation in the ABP. The dCA in both the MCA and PCA remained unaltered at CPT. These findings suggest that CPT-induced elevations in the ABP and SNA did not cause changes in the CBF regulation in the posterior circulation compared with the anterior circulation.
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Affiliation(s)
- Takuro Washio
- Department of Biomedical Engineering, Toyo University, 2100 Kujirai, Kawagoe-shi, Saitama, 350-8585, Japan
- Research Fellow of Japan Society for the Promotion of Science, Tokyo, Japan
| | - Hironori Watanabe
- Department of Biomedical Engineering, Toyo University, 2100 Kujirai, Kawagoe-shi, Saitama, 350-8585, Japan
| | - Shigehiko Ogoh
- Department of Biomedical Engineering, Toyo University, 2100 Kujirai, Kawagoe-shi, Saitama, 350-8585, Japan.
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Duyn JH, Ozbay PS, Chang C, Picchioni D. Physiological changes in sleep that affect fMRI inference. Curr Opin Behav Sci 2019; 33:42-50. [PMID: 32613032 DOI: 10.1016/j.cobeha.2019.12.007] [Citation(s) in RCA: 21] [Impact Index Per Article: 3.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/13/2022]
Abstract
fMRI relies on a localized cerebral blood flow (CBF) response to changes in cortical neuronal activity. An underappreciated aspect however is its sensitivity to contributions from autonomic physiology that may affect CBF through changes in vascular resistance and blood pressure. As is reviewed here, this is crucial to consider in fMRI studies of sleep, given the close linkage between the regulation of arousal state and autonomic physiology. Typical methods for separating these effects are based on the use of reference signals that may include physiological parameters such as heart rate and respiration; however, the use of time-invariant models may not be adequate due to the possibly changing relationship between reference and fMRI signals with arousal state. In addition, recent research indicates that additional physiological reference signals may be needed to accurately describe changes in systemic physiology, including sympathetic indicators such as finger skin vascular tone and blood pressure.
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Affiliation(s)
- Jeff H Duyn
- Advanced Magnetic Resonance Imaging Section, National Institute of Neurological Disorders and Stroke
| | - Pinar S Ozbay
- Advanced Magnetic Resonance Imaging Section, National Institute of Neurological Disorders and Stroke
| | - Catie Chang
- Department of Electrical Engineering and Computer Science, Vanderbilt University
| | - Dante Picchioni
- Advanced Magnetic Resonance Imaging Section, National Institute of Neurological Disorders and Stroke
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Özbay PS, Chang C, Picchioni D, Mandelkow H, Chappel-Farley MG, van Gelderen P, de Zwart JA, Duyn J. Sympathetic activity contributes to the fMRI signal. Commun Biol 2019; 2:421. [PMID: 31754651 PMCID: PMC6861267 DOI: 10.1038/s42003-019-0659-0] [Citation(s) in RCA: 51] [Impact Index Per Article: 8.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/23/2019] [Accepted: 10/21/2019] [Indexed: 12/15/2022] Open
Abstract
The interpretation of functional magnetic resonance imaging (fMRI) studies of brain activity is often hampered by the presence of brain-wide signal variations that may arise from a variety of neuronal and non-neuronal sources. Recent work suggests a contribution from the sympathetic vascular innervation, which may affect the fMRI signal through its putative and poorly understood role in cerebral blood flow (CBF) regulation. By analyzing fMRI and (electro-) physiological signals concurrently acquired during sleep, we found that widespread fMRI signal changes often co-occur with electroencephalography (EEG) K-complexes, signatures of sub-cortical arousal, and episodic drops in finger skin vascular tone; phenomena that have been associated with intermittent sympathetic activity. These findings support the notion that the extrinsic sympathetic innervation of the cerebral vasculature contributes to CBF regulation and the fMRI signal. Accounting for this mechanism could help separate systemic from local signal contributions and improve interpretation of fMRI studies.
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Affiliation(s)
- Pinar Senay Özbay
- Advanced MRI Section, LFMI, NINDS, National Institutes of Health, Bethesda, MD USA
| | | | - Dante Picchioni
- Advanced MRI Section, LFMI, NINDS, National Institutes of Health, Bethesda, MD USA
| | - Hendrik Mandelkow
- Advanced MRI Section, LFMI, NINDS, National Institutes of Health, Bethesda, MD USA
| | | | - Peter van Gelderen
- Advanced MRI Section, LFMI, NINDS, National Institutes of Health, Bethesda, MD USA
| | | | - Jeff Duyn
- Advanced MRI Section, LFMI, NINDS, National Institutes of Health, Bethesda, MD USA
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10
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Ogoh S. Interaction between the respiratory system and cerebral blood flow regulation. J Appl Physiol (1985) 2019; 127:1197-1205. [PMID: 30920887 DOI: 10.1152/japplphysiol.00057.2019] [Citation(s) in RCA: 19] [Impact Index Per Article: 3.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/22/2022] Open
Abstract
This review summarizes the interaction between the regulatory system of respiration and cerebral vasculature. Some clinical reports provide evidence for the association between these two physiological regulatory systems. Physiologically, arterial carbon dioxide concentration is mainly regulated by two feedback control systems: respiration and cerebral blood flow. In other words, both of these systems are sensitive to the same mediator, i.e., carbon dioxide, at a set point. In addition, respiratory dysfunction alters various physiological factors that affect the cerebral vasculature. Therefore, it is physiologically plausible that these systems are closely linked. The regulation of arterial carbon dioxide concentration affected by respiration and cerebral blood flow may be a key factor for a rise in the risk of brain disease in the patients with respiratory dysfunction. For example, the management of respiratory disease (e.g., patients with chronic obstructive pulmonary disease) and the use of prophylactic therapy are essential to reduce the risk of stroke.
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Affiliation(s)
- Shigehiko Ogoh
- Department of Biomedical Engineering, Toyo University, Kawagoe-Shi, Saitama, Japan
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11
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Zheng S, Muheremu A, Sun Y, Tian W, Wu CA. Preoperative imaging differences of patients with cervical spondylosis with cervical vertigo indicate the prognosis after cervical total disc replacement. J Int Med Res 2019; 48:300060519877033. [PMID: 31640443 PMCID: PMC7607185 DOI: 10.1177/0300060519877033] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/16/2022] Open
Abstract
OBJECTIVE To evaluate the relationship between the preoperative imaging differences and prognosis in patients with cervical spondylosis with cervical vertigo who underwent total disc replacement (TDR). METHODS This was a retrospective study of patients with cervical spondylosis with cervical vertigo treated with single-segment TDR. The severity of pre- and postoperative cervical vertigo was evaluated separately. Paired samples t-tests were used to compare the severity of the symptoms before and after surgery. Characteristics of plain films, computed tomography myelography and magnetic resonance imaging were compared between patients with different outcomes by analysis of variance and Fisher's exact tests. RESULTS The severity of cervical vertigo was significantly different after single-segment TDR. Three groups with different treatment outcomes were not significantly different with regard to gender, age, type of the cervical spondylosis, follow-up time, segment of surgery, cervical curve, range of motion, T2WI high signal in the spinal cord, and location of compression. The type of compression was significantly different between the three groups. CONCLUSIONS Cervical vertigo was improved in patients with cervical spondylosis through the TDR procedure. Those in whom a herniated disc was the main source of compression may have a better prognosis following TDR.
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Affiliation(s)
- Shan Zheng
- Department of Spine Surgery, Beijing Jishuitan Hospital, Beijing, China
| | | | - Yuqing Sun
- Department of Spine Surgery, Beijing Jishuitan Hospital, Beijing, China
| | - Wei Tian
- Department of Spine Surgery, Beijing Jishuitan Hospital, Beijing, China
| | - Cheng-Ai Wu
- Department of Molecular Orthopaedics, Beijing Institute of Traumatology and Orthopaedics, Beijing, China
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12
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Becker BK, Zhang D, Soliman R, Pollock DM. Autonomic nerves and circadian control of renal function. Auton Neurosci 2019; 217:58-65. [PMID: 30704976 PMCID: PMC6415626 DOI: 10.1016/j.autneu.2019.01.003] [Citation(s) in RCA: 7] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/08/2018] [Revised: 01/07/2019] [Accepted: 01/09/2019] [Indexed: 12/12/2022]
Abstract
Cardiovascular and renal physiology follow strong circadian rhythms. For instance, renal excretion of solutes and water is higher during the active period compared to the inactive period, and blood pressure peaks early in the beginning of the active period of both diurnal and nocturnal animals. The control of these rhythms is largely dependent on the expression of clock genes both in the central nervous system and within peripheral organs themselves. Although it is understood that the central and peripheral clocks interact and communicate, few studies have explored the specific mechanism by which various organ systems within the body are coordinated to control physiological processes. The renal sympathetic nervous innervation has long been known to have profound effects on renal function, and because the sympathetic nervous system follows strong circadian rhythms, it is likely that autonomic control of the kidney plays an integral role in modulating renal circadian function. This review highlights studies that provide insight into this interaction, discusses areas lacking clarity, and suggests the potential for future work to explore the role of renal autonomics in areas such as blood pressure control and chronic kidney disease.
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Affiliation(s)
- Bryan K Becker
- Section of Cardio-Renal Physiology and Medicine, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, United States of America
| | - Dingguo Zhang
- Section of Cardio-Renal Physiology and Medicine, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, United States of America
| | - Reham Soliman
- Section of Cardio-Renal Physiology and Medicine, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, United States of America
| | - David M Pollock
- Section of Cardio-Renal Physiology and Medicine, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, United States of America.
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Devaraja K. Approach to cervicogenic dizziness: a comprehensive review of its aetiopathology and management. Eur Arch Otorhinolaryngol 2018; 275:2421-2433. [PMID: 30094486 DOI: 10.1007/s00405-018-5088-z] [Citation(s) in RCA: 37] [Impact Index Per Article: 5.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/29/2018] [Accepted: 08/06/2018] [Indexed: 02/07/2023]
Abstract
PURPOSE Though there is abundant literature on cervicogenic dizziness with at least half a dozen of review articles, the condition remains to be enigmatic for clinicians dealing with the dizzy patients. However, most of these studies have studied the cervicogenic dizziness in general without separating the constitute conditions. Since the aetiopathological mechanism of dizziness varies between these cervicogenic causes, one cannot rely on the universal conclusions of these studies unless the constitute conditions of cervicogenic dizziness are separated and contrasted against each other. METHODS This narrative review of recent literature revisits the pathophysiology and the management guidelines of various conditions causing the cervicogenic dizziness, with an objective to formulate a practical algorithm that could be of clinical utility. The structured discussion on each of the causes of the cervicogenic dizziness not only enhances the readers' understanding of the topic in depth but also enables further research by identifying the potential areas of interest and the missing links. RESULTS Certain peculiar features of each condition have been discussed with an emphasis on the recent experimental and clinical studies. A simple aetiopathological classification and a sensible management algorithm have been proposed by the author, to enable the identification of the most appropriate underlying cause for the cervicogenic dizziness in any given case. However, further clinical studies are required to validate this algorithm. CONCLUSIONS So far, no single clinical study, either epidemiological or interventional, has incorporated and isolated all the constitute conditions of cervicogenic dizziness. There is a need for such studies in the future to validate either the reliability of a clinical test or the efficacy of an intervention in cervicogenic dizziness.
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Affiliation(s)
- K Devaraja
- Department of Otorhinolaryngology, Kasturba Medical College, Manipal Academy of Higher Education, Manipal, Udupi, Karnataka, 576104, India.
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Roloff EVL, Tomiak‐Baquero AM, Kasparov S, Paton JFR. Parasympathetic innervation of vertebrobasilar arteries: is this a potential clinical target? J Physiol 2016; 594:6463-6485. [PMID: 27357059 PMCID: PMC5108906 DOI: 10.1113/jp272450] [Citation(s) in RCA: 33] [Impact Index Per Article: 3.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/17/2016] [Accepted: 06/18/2016] [Indexed: 12/25/2022] Open
Abstract
This review aims to summarise the contemporary evidence for the presence and function of the parasympathetic innervation of the cerebral circulation with emphasis on the vertebral and basilar arteries (the posterior cerebral circulation). We consider whether the parasympathetic innervation of blood vessels could be used as a means to increase cerebral blood flow. This may have clinical implications for pathologies associated with cerebral hypoperfusion such as stroke, dementia and hypertension. Relative to the anterior cerebral circulation little is known of the origins and neurochemical phenotypes of the parasympathetic innervation of the vertebrobasilar arteries. These vessels normally provide blood flow to the brainstem and cerebellum but can, via the Circle of Willis upon stenosis of the internal carotid arteries, supply blood to the anterior cerebral circulation too. We review the multiple types of parasympathetic fibres and their distinct transmitter mechanisms and how these vary with age, disease and species. We highlight the importance of parasympathetic fibres for mediating the vasodilatory response to sympathetic activation. Current trials are investigating the possibility of electrically stimulating the postganglionic parasympathetic ganglia to improve cerebal blood flow to reduce the penumbra following stroke. We conclude that although there are substantial gaps in our understanding of the origins of parasympathetic innervation of the vertebrobasilar arteries, activation of this system under some conditions might bring therapeutic benefits.
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Affiliation(s)
- Eva v. L. Roloff
- School of Physiology, Pharmacology and Neuroscience, Biomedical SciencesUniversity of BristolBristolBS8 1TDUK
| | - Ana M. Tomiak‐Baquero
- School of Physiology, Pharmacology and Neuroscience, Biomedical SciencesUniversity of BristolBristolBS8 1TDUK
| | - Sergey Kasparov
- School of Physiology, Pharmacology and Neuroscience, Biomedical SciencesUniversity of BristolBristolBS8 1TDUK
| | - Julian F. R. Paton
- School of Physiology, Pharmacology and Neuroscience, Biomedical SciencesUniversity of BristolBristolBS8 1TDUK
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15
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Ogoh S, Sørensen H, Hirasawa A, Sasaki H, Washio T, Hashimoto T, Bailey DM, Secher NH. Dynamic cerebral autoregulation is unrelated to decrease in external carotid artery blood flow during acute hypotension in healthy young men. Exp Physiol 2016; 101:1040-9. [PMID: 27228963 DOI: 10.1113/ep085772] [Citation(s) in RCA: 12] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/01/2016] [Accepted: 05/19/2016] [Indexed: 11/08/2022]
Abstract
NEW FINDINGS What is the central question of this study? Dynamic cerebral autoregulation (CA) is impaired by sympathetic blockade, and the external carotid artery (ECA) vascular bed may prevent adequate internal carotid artery blood flow. We examined whether α1 -receptor blockade-induced attenuation of dynamic CA is related to reduced ECA vasoconstriction. What is the main finding and its importance? α1 -Receptor blockade attenuated dynamic CA, but in contrast to our hypothesis did not affect the ECA blood flow response to acute hypotension. These findings suggest that the recovery of cerebral blood flow during acute hypotension is unrelated to vasoconstriction within the ECA territory. External carotid artery (ECA) vasoconstriction may defend internal carotid artery (ICA) blood flow during acute hypotension. We hypothesized that the α1 -receptor blockade-induced delay in ICA recovery to the baseline level from acute hypoperfusion is related to attenuated ECA vasoconstriction. The ICA and ECA blood flow were determined by duplex ultrasound during thigh-cuff release-induced acute hypotension while the α1 -receptor blocker prazosin [1 mg (20 kg)(-1) ] was administered to nine seated young healthy men. Both ICA (mean ± SD; by 17 ± 8%, P = 0.005) and ECA (by 37 ± 15%, P < 0.001) blood flow decreased immediately after occluded thigh-cuff release, with a more rapid ICA blood flow recovery to the baseline level (9 ± 5 s) than for the ECA blood flow (17 ± 5 s; P = 0.019). The ICA blood flow recovery from hypoperfusion was delayed with prazosin (17 ± 4 s versus control 9 ± 5 s, P = 0.006), whereas ECA recovery remained unchanged (P = 0.313) despite a similar reduction in mean arterial pressure (-20 ± 4 mmHg versus control -23 ± 7 mmHg, P = 0.148). These findings suggest that α1 -receptor blockade-induced attenuation of the ICA blood flow response to acute hypotension is unrelated to the reduction in ECA blood flow. The sympathetic nervous system via the ECA vascular bed does not contribute to dynamic CA during acute hypotension.
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Affiliation(s)
- Shigehiko Ogoh
- Department of Biomedical Engineering, Toyo University, Kawagoe-Shi, Saitama, Japan
| | - Henrik Sørensen
- The Copenhagen Muscle Research Centre, Department of Anesthesia, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
| | - Ai Hirasawa
- Advanced Triage Team, Kyorin University School of Medicine, Mitaka-Shi, Tokyo, Japan
| | - Hiroyuki Sasaki
- Department of Biomedical Engineering, Toyo University, Kawagoe-Shi, Saitama, Japan
| | - Takuro Washio
- Department of Biomedical Engineering, Toyo University, Kawagoe-Shi, Saitama, Japan
| | - Takeshi Hashimoto
- Graduate School of Sport and Health Science, Ritsumeikan University, Shiga, Japan
| | - Damian M Bailey
- Neurovascular Research Laboratory, Research Institute of Health and Wellbeing, Faculty of Life Sciences and Education, University of South Wales, UK
| | - Niels H Secher
- The Copenhagen Muscle Research Centre, Department of Anesthesia, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
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16
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Phillips AA, Chan FH, Zheng MMZ, Krassioukov AV, Ainslie PN. Neurovascular coupling in humans: Physiology, methodological advances and clinical implications. J Cereb Blood Flow Metab 2016; 36:647-64. [PMID: 26661243 PMCID: PMC4821024 DOI: 10.1177/0271678x15617954] [Citation(s) in RCA: 316] [Impact Index Per Article: 35.1] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/11/2015] [Revised: 10/22/2015] [Accepted: 10/23/2015] [Indexed: 12/16/2022]
Abstract
Neurovascular coupling reflects the close temporal and regional linkage between neural activity and cerebral blood flow. Although providing mechanistic insight, our understanding of neurovascular coupling is largely limited to non-physiologicalex vivopreparations and non-human models using sedatives/anesthetics with confounding cerebrovascular implications. Herein, with particular focus on humans, we review the present mechanistic understanding of neurovascular coupling and highlight current approaches to assess these responses and the application in health and disease. Moreover, we present new guidelines for standardizing the assessment of neurovascular coupling in humans. To improve the reliability of measurement and related interpretation, the utility of new automated software for neurovascular coupling is demonstrated, which provides the capacity for coalescing repetitive trials and time intervals into single contours and extracting numerous metrics (e.g., conductance and pulsatility, critical closing pressure, etc.) according to patterns of interest (e.g., peak/minimum response, time of response, etc.). This versatile software also permits the normalization of neurovascular coupling metrics to dynamic changes in arterial blood gases, potentially influencing the hyperemic response. It is hoped that these guidelines, combined with the newly developed and openly available software, will help to propel the understanding of neurovascular coupling in humans and also lead to improved clinical management of this critical physiological function.
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Affiliation(s)
- Aaron A Phillips
- Centre for Heart, Lung and Vascular Health, School of Health and Exercise Sciences, University of British Columbia - Okanagan, Kelowna, British Columbia, Canada International Collaboration on Repair Discoveries (ICORD), UBC, Vancouver, Canada Experimental Medicine Program, Faculty of Medicine, UBC, Vancouver, Canada
| | - Franco Hn Chan
- International Collaboration on Repair Discoveries (ICORD), UBC, Vancouver, Canada
| | - Mei Mu Zi Zheng
- International Collaboration on Repair Discoveries (ICORD), UBC, Vancouver, Canada Experimental Medicine Program, Faculty of Medicine, UBC, Vancouver, Canada
| | - Andrei V Krassioukov
- International Collaboration on Repair Discoveries (ICORD), UBC, Vancouver, Canada Experimental Medicine Program, Faculty of Medicine, UBC, Vancouver, Canada Department of Physical Therapy, UBC, Vancouver, Canada GF Strong Rehabilitation Center, Vancouver, Canada Department of Medicine, Division of Physical Medicine and Rehabilitation, UBC, Vancouver, Canada
| | - Philip N Ainslie
- Centre for Heart, Lung and Vascular Health, School of Health and Exercise Sciences, University of British Columbia - Okanagan, Kelowna, British Columbia, Canada
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17
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Peng B, Pang X, Li D, Yang H. Cervical spondylosis and hypertension: a clinical study of 2 cases. Medicine (Baltimore) 2015; 94:e618. [PMID: 25761188 PMCID: PMC4602471 DOI: 10.1097/md.0000000000000618] [Citation(s) in RCA: 20] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/27/2015] [Revised: 02/10/2015] [Accepted: 02/11/2015] [Indexed: 12/26/2022] Open
Abstract
Cervical spondylosis and hypertension are all common diseases, but the relationship between them has never been studied. Patients with cervical spondylosis are often accompanied with vertigo. Anterior cervical discectomy and fusion is an effective method of treatment for cervical spondylosis with cervical vertigo that is unresponsive to conservative therapy. We report 2 patients of cervical spondylosis with concomitant cervical vertigo and hypertension who were treated successfully with anterior cervical discectomy and fusion. Stimulation of sympathetic nerve fibers in pathologically degenerative disc could produce sympathetic excitation, and induce a sympathetic reflex to cause cervical vertigo and hypertension. In addition, chronic neck pain could contribute to hypertension development through sympathetic arousal and failure of normal homeostatic pain regulatory mechanisms. Cervical spondylosis may be one of the causes of secondary hypertension. Early treatment for resolution of symptoms of cervical spondylosis may have a beneficial impact on cardiovascular disease risk in patients with cervical spondylosis.
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Affiliation(s)
- Baogan Peng
- From the Department of Spinal Surgery, General Hospital of Armed Police Force, Beijing, China
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18
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Bain AR, Morrison SA, Ainslie PN. Cerebral oxygenation and hyperthermia. Front Physiol 2014; 5:92. [PMID: 24624095 PMCID: PMC3941303 DOI: 10.3389/fphys.2014.00092] [Citation(s) in RCA: 28] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/09/2014] [Accepted: 02/18/2014] [Indexed: 12/04/2022] Open
Abstract
Hyperthermia is associated with marked reductions in cerebral blood flow (CBF). Increased distribution of cardiac output to the periphery, increases in alveolar ventilation and resultant hypocapnia each contribute to the fall in CBF during passive hyperthermia; however, their relative contribution remains a point of contention, and probably depends on the experimental condition (e.g., posture and degree of hyperthermia). The hyperthermia-induced hyperventilatory response reduces arterial CO2 pressure (PaCO2) causing cerebral vasoconstriction and subsequent reductions in flow. During supine passive hyperthermia, the majority of recent data indicate that reductions in PaCO2 may be the primary, if not sole, culprit for reduced CBF. On the other hand, during more dynamic conditions (e.g., hemorrhage or orthostatic challenges), an inability to appropriately decrease peripheral vascular conductance presents a condition whereby adequate cerebral perfusion pressure may be compromised secondary to reductions in systemic blood pressure. Although studies have reported maintenance of pre-frontal cortex oxygenation (assessed by near-infrared spectroscopy) during exercise and severe heat stress, the influence of cutaneous blood flow is known to contaminate this measure. This review discusses the governing mechanisms associated with changes in CBF and oxygenation during moderate to severe (i.e., 1.0°C to 2.0°C increase in body core temperature) levels of hyperthermia. Future research directions are provided.
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Affiliation(s)
- Anthony R Bain
- Centre for Heart Lung and Vascular Health, University of British Columbia Okanagan, BC, Canada
| | - Shawnda A Morrison
- Faculty of Professional Studies, Kinesiology, Acadia University Wolfville, NS, Canada
| | - Philip N Ainslie
- Centre for Heart Lung and Vascular Health, University of British Columbia Okanagan, BC, Canada
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19
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Ainslie PN, Brassard P. Why is the neural control of cerebral autoregulation so controversial? F1000PRIME REPORTS 2014; 6:14. [PMID: 24669295 PMCID: PMC3944747 DOI: 10.12703/p6-14] [Citation(s) in RCA: 70] [Impact Index Per Article: 6.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Subscribe] [Scholar Register] [Indexed: 12/20/2022]
Abstract
Cerebral autoregulation refers to the mechanisms that act to keep cerebral blood flow (CBF) constant during changes in blood pressure. The mechanisms of cerebral autoregulation, especially in humans, are poorly understood but are undoubtedly multifactorial and likely reflect many redundant pathways that potentially differ between species. Whether sympathetic nervous activity influences CBF and/or cerebral autoregulation in humans remains controversial. Following a brief introduction to cerebral autoregulation, this review highlights the likely reasons behind the controversy of the neural control of cerebral autoregulation. Finally, suggestions are provided for further studies to improve the understanding of the neural control of CBF regulation.
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Affiliation(s)
- Philip N. Ainslie
- Center for Heart, Lung and Vascular Health, School of Health and Exercise Sciences, University of British Columbia – OkanaganKelowna, British ColumbiaCanada
| | - Patrice Brassard
- Department of Kinesiology, Faculty of Medicine, Université LavalQuébecCanada
- Research Center of the Institut Universitaire de Cardiologie et de Pneumologie de QuébecQuébecCanada
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20
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Willie CK, Tzeng YC, Fisher JA, Ainslie PN. Integrative regulation of human brain blood flow. J Physiol 2014; 592:841-59. [PMID: 24396059 PMCID: PMC3948549 DOI: 10.1113/jphysiol.2013.268953] [Citation(s) in RCA: 622] [Impact Index Per Article: 56.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/26/2013] [Accepted: 12/24/2013] [Indexed: 02/06/2023] Open
Abstract
Herein, we review mechanisms regulating cerebral blood flow (CBF), with specific focus on humans. We revisit important concepts from the older literature and describe the interaction of various mechanisms of cerebrovascular control. We amalgamate this broad scope of information into a brief review, rather than detailing any one mechanism or area of research. The relationship between regulatory mechanisms is emphasized, but the following three broad categories of control are explicated: (1) the effect of blood gases and neuronal metabolism on CBF; (2) buffering of CBF with changes in blood pressure, termed cerebral autoregulation; and (3) the role of the autonomic nervous system in CBF regulation. With respect to these control mechanisms, we provide evidence against several canonized paradigms of CBF control. Specifically, we corroborate the following four key theses: (1) that cerebral autoregulation does not maintain constant perfusion through a mean arterial pressure range of 60-150 mmHg; (2) that there is important stimulatory synergism and regulatory interdependence of arterial blood gases and blood pressure on CBF regulation; (3) that cerebral autoregulation and cerebrovascular sensitivity to changes in arterial blood gases are not modulated solely at the pial arterioles; and (4) that neurogenic control of the cerebral vasculature is an important player in autoregulatory function and, crucially, acts to buffer surges in perfusion pressure. Finally, we summarize the state of our knowledge with respect to these areas, outline important gaps in the literature and suggest avenues for future research.
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Affiliation(s)
- Christopher K Willie
- Centre for Heart, Lung and Vascular Health, School of Health and Exercise Sciences, University of British Columbia - Okanagan, Kelowna, British Columbia, Canada V1V 1V7.
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21
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Laughlin MH, Davis MJ, Secher NH, van Lieshout JJ, Arce-Esquivel AA, Simmons GH, Bender SB, Padilla J, Bache RJ, Merkus D, Duncker DJ. Peripheral circulation. Compr Physiol 2013; 2:321-447. [PMID: 23728977 DOI: 10.1002/cphy.c100048] [Citation(s) in RCA: 182] [Impact Index Per Article: 15.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]
Abstract
Blood flow (BF) increases with increasing exercise intensity in skeletal, respiratory, and cardiac muscle. In humans during maximal exercise intensities, 85% to 90% of total cardiac output is distributed to skeletal and cardiac muscle. During exercise BF increases modestly and heterogeneously to brain and decreases in gastrointestinal, reproductive, and renal tissues and shows little to no change in skin. If the duration of exercise is sufficient to increase body/core temperature, skin BF is also increased in humans. Because blood pressure changes little during exercise, changes in distribution of BF with incremental exercise result from changes in vascular conductance. These changes in distribution of BF throughout the body contribute to decreases in mixed venous oxygen content, serve to supply adequate oxygen to the active skeletal muscles, and support metabolism of other tissues while maintaining homeostasis. This review discusses the response of the peripheral circulation of humans to acute and chronic dynamic exercise and mechanisms responsible for these responses. This is accomplished in the context of leading the reader on a tour through the peripheral circulation during dynamic exercise. During this tour, we consider what is known about how each vascular bed controls BF during exercise and how these control mechanisms are modified by chronic physical activity/exercise training. The tour ends by comparing responses of the systemic circulation to those of the pulmonary circulation relative to the effects of exercise on the regional distribution of BF and mechanisms responsible for control of resistance/conductance in the systemic and pulmonary circulations.
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Affiliation(s)
- M Harold Laughlin
- Department of Medical Pharmacology and Physiology, and the Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri, USA.
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Bolduc V, Thorin-Trescases N, Thorin E. Endothelium-dependent control of cerebrovascular functions through age: exercise for healthy cerebrovascular aging. Am J Physiol Heart Circ Physiol 2013; 305:H620-33. [PMID: 23792680 DOI: 10.1152/ajpheart.00624.2012] [Citation(s) in RCA: 75] [Impact Index Per Article: 6.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/17/2023]
Abstract
Cognitive performances are tightly associated with the maximal aerobic exercise capacity, both of which decline with age. The benefits on mental health of regular exercise, which slows the age-dependent decline in maximal aerobic exercise capacity, have been established for centuries. In addition, the maintenance of an optimal cerebrovascular endothelial function through regular exercise, part of a healthy lifestyle, emerges as one of the key and primary elements of successful brain aging. Physical exercise requires the activation of specific brain areas that trigger a local increase in cerebral blood flow to match neuronal metabolic needs. In this review, we propose three ways by which exercise could maintain the cerebrovascular endothelial function, a premise to a healthy cerebrovascular function and an optimal regulation of cerebral blood flow. First, exercise increases blood flow locally and increases shear stress temporarily, a known stimulus for endothelial cell maintenance of Akt-dependent expression of endothelial nitric oxide synthase, nitric oxide generation, and the expression of antioxidant defenses. Second, the rise in circulating catecholamines during exercise not only facilitates adequate blood and nutrient delivery by stimulating heart function and mobilizing energy supplies but also enhances endothelial repair mechanisms and angiogenesis. Third, in the long term, regular exercise sustains a low resting heart rate that reduces the mechanical stress imposed to the endothelium of cerebral arteries by the cardiac cycle. Any chronic variation from a healthy environment will perturb metabolism and thus hasten endothelial damage, favoring hypoperfusion and neuronal stress.
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Affiliation(s)
- Virginie Bolduc
- Departments of Surgery and Pharmacology, Université de Montréal, and Centre de recherche, Montreal Heart Institute, Montreal, Quebec, Canada
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23
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Westcott EB, Segal SS. Ageing alters perivascular nerve function of mouse mesenteric arteries in vivo. J Physiol 2013; 591:1251-63. [PMID: 23247111 PMCID: PMC3607869 DOI: 10.1113/jphysiol.2012.244483] [Citation(s) in RCA: 20] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/04/2012] [Accepted: 12/10/2012] [Indexed: 12/16/2022] Open
Abstract
Abstract Mesenteric arteries (MAs) are studied widely in vitro but little is known of their reactivity in vivo. Transgenic animals have enabled Ca(2+) signalling to be studied in isolated MAs but the reactivity of these vessels in vivo is undefined. We tested the hypothesis that ageing alters MA reactivity to perivascular nerve stimulation (PNS) and adrenoreceptor (AR) activation during blood flow control. First- (1A), second- (2A) and third-order (3A) MAs of pentobarbital-anaesthetized Young (3-6 months) and Old (24-26 months) male and female Cx40(BAC)-GCaMP2 transgenic mice (C57BL/6 background; positive or negative for the GCaMP2 transgene) were studied with intravital microscopy. A segment of jejunum was exteriorized and an MA network was superfused with physiological salt solution (pH 7.4, 37°C). Resting tone was 10% in MAs of Young and Old mice; diameters were ∼5% (1A), 20% (2A) and 40% (3A) smaller (P 0.05) in Old mice. Throughout MA networks, vasoconstriction increased with PNS frequency (1-16 Hz) but was ∼20% less in Young vs. Old mice (P 0.05) and was inhibited by tetrodotoxin (1 μm). Capsaicin (10 μm; to inhibit sensory nerves) enhanced MA constriction to PNS (P 0.05) by ∼20% in Young but not Old mice. Phenylephrine (an α1AR agonist) potency was greater in Young mice (P 0.05) with similar efficacy (∼60% constriction) across ages and MA branches. Constrictions to UK14304 (an α2AR agonist) were less (∼20%; P 0.05) and were unaffected by ageing. Irrespective of sex or transgene expression, ageing consistently reduced the sensitivity of MAs to α1AR vasoconstriction while blunting the attenuation of sympathetic vasoconstriction by sensory nerves. These findings imply substantive alterations in splanchnic blood flow control with ageing.
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Affiliation(s)
- Erika B Westcott
- Department of Medical Pharmacology and Physiology, University of Missouri, Columbia, MO 65212, USA
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24
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Purkayastha S, Raven PB. The functional role of the alpha-1 adrenergic receptors in cerebral blood flow regulation. Indian J Pharmacol 2011; 43:502-6. [PMID: 22021989 PMCID: PMC3195116 DOI: 10.4103/0253-7613.84950] [Citation(s) in RCA: 26] [Impact Index Per Article: 1.9] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/04/2011] [Revised: 05/11/2011] [Accepted: 07/01/2011] [Indexed: 01/22/2023] Open
Abstract
Cerebral vasculature is richly innervated by the α-1 adrenergic receptors similar to that of the peripheral vasculature. However, the functional role of the α-1adrenergic receptors in cerebral blood flow (CBF) regulation is yet to be established. The traditional thinking being that during normotension and normocapnia sympathetic neural activity does not play a significant role in CBF regulation. Reports in the past have stated that catecholamines do not penetrate the blood brain barrier (BBB) and therefore only influence cerebral vessels from outside the BBB and hence, have a limited role in CBF regulation. However, with the advent of dynamic measurement techniques, beat-to-beat CBF assessment can be done during dynamic changes in arterial blood pressure. Several studies in the recent years have reported a functional role of the α-1adrenergic receptors in CBF regulation. This review focuses on the recent developments on the role of the sympathetic nervous system, specifically that of the α-1 adrenergic receptors in CBF regulation.
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Affiliation(s)
- Sushmita Purkayastha
- Department of Integrative Physiology and the Cardiovascular Research Institute, University of North Texas Health Science Center, Fort Worth, Texas, 76017, USA
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Sato K, Ogoh S, Hirasawa A, Oue A, Sadamoto T. The distribution of blood flow in the carotid and vertebral arteries during dynamic exercise in humans. J Physiol 2011; 589:2847-56. [PMID: 21486813 DOI: 10.1113/jphysiol.2010.204461] [Citation(s) in RCA: 212] [Impact Index Per Article: 15.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/08/2022] Open
Abstract
The mechanism underlying the plateau or relative decrease in cerebral blood flow (CBF) during maximal incremental dynamic exercise remains unclear. We hypothesized that cerebral perfusion is limited during high-intensity dynamic exercise due to a redistribution of carotid artery blood flow. To identify the distribution of blood flow among the arteries supplying the head and brain, we evaluated common carotid artery (CCA), internal carotid artery (ICA), external carotid artery (ECA) and vertebral artery (VA) blood flow during dynamic exercise using Doppler ultrasound. Ten subjects performed graded cycling exercise in a semi-supine position at 40, 60 and 80% of peak oxygen uptake (VO2 peak) for 5 min at each workload. The ICA blood flow increased by 23.0 ± 4.6% (mean ± SE) from rest to exercise at 60% (VO2 peak). However, at 80% (VO2 peak), ICA blood flow returned towards near resting levels (9.6 ± 4.7% vs. rest). In contrast, ECA, CCA and VA blood flow increased proportionally with workload. The change in ICA blood flow during graded exercise was correlated with end-tidal partial pressure of CO2 (r = 0.72). The change in ICA blood flow from 60% (VO2 peak) to 80% (VO2 peak) was negatively correlated with the change in ECA blood flow (r = −0.77). Moreover, there was a significant correlation between forehead cutaneous vascular conductance and ECA blood flow during exercise (r = 0.79). These results suggest that during high-intensity dynamic exercise the plateau or decrease in ICA blood flow is partly due to a large increase in ECA blood flow, which is selectively increased to prioritize thermoregulation.
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Affiliation(s)
- Kohei Sato
- Research Institute of Physical Fitness, Japan Women's College of Physical Education, Kita-Karasuyama, Setagaya-ku, Tokyo 157-8565, Japan.
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Ogoh S, Fisher JP, Young CN, Fadel PJ. Impact of age on critical closing pressure of the cerebral circulation during dynamic exercise in humans. Exp Physiol 2011; 96:417-25. [DOI: 10.1113/expphysiol.2010.055871] [Citation(s) in RCA: 13] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/08/2022]
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Ogoh S, Brothers RM, Jeschke M, Secher NH, Raven PB. Estimation of cerebral vascular tone during exercise; evaluation by critical closing pressure in humans. Exp Physiol 2010; 95:678-85. [DOI: 10.1113/expphysiol.2010.052340] [Citation(s) in RCA: 20] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/08/2022]
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Ogoh S, Ainslie PN. Cerebral blood flow during exercise: mechanisms of regulation. J Appl Physiol (1985) 2009; 107:1370-80. [PMID: 19729591 DOI: 10.1152/japplphysiol.00573.2009] [Citation(s) in RCA: 368] [Impact Index Per Article: 23.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/22/2022] Open
Abstract
The response of cerebral vasculature to exercise is different from other peripheral vasculature; it has a small vascular bed and is strongly regulated by cerebral autoregulation and the partial pressure of arterial carbon dioxide (Pa(CO(2))). In contrast to other organs, the traditional thinking is that total cerebral blood flow (CBF) remains relatively constant and is largely unaffected by a variety of conditions, including those imposed during exercise. Recent research, however, indicates that cerebral neuronal activity and metabolism drive an increase in CBF during exercise. Increases in exercise intensity up to approximately 60% of maximal oxygen uptake produce elevations in CBF, after which CBF decreases toward baseline values because of lower Pa(CO(2)) via hyperventilation-induced cerebral vasoconstriction. This finding indicates that, during heavy exercise, CBF decreases despite the cerebral metabolic demand. In contrast, this reduced CBF during heavy exercise lowers cerebral oxygenation and therefore may act as an independent influence on central fatigue. In this review, we highlight methodological considerations relevant for the assessment of CBF and then summarize the integrative mechanisms underlying the regulation of CBF at rest and during exercise. In addition, we examine how CBF regulation during exercise is altered by exercise training, hypoxia, and aging and suggest avenues for future research.
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Affiliation(s)
- Shigehiko Ogoh
- Dept. of Biomedical Engineering, Toyo Univ., 2100 Kujirai, Kawagoe-shi, Saitama 350-8585, Japan.
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Cassaglia PA, Griffiths RI, Walker AM. Cerebral sympathetic nerve activity has a major regulatory role in the cerebral circulation in REM sleep. J Appl Physiol (1985) 2009; 106:1050-6. [DOI: 10.1152/japplphysiol.91349.2008] [Citation(s) in RCA: 51] [Impact Index Per Article: 3.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/22/2022] Open
Abstract
Sympathetic nerve activity (SNA) in neurons projecting to skeletal muscle blood vessels increases during rapid-eye-movement (REM) sleep, substantially exceeding SNA of non-REM (NREM) sleep and quiet wakefulness (QW). Similar SNA increases to cerebral blood vessels may regulate the cerebral circulation in REM sleep, but this is unknown. We hypothesized that cerebral SNA increases during phasic REM sleep, constricting cerebral vessels as a protective mechanism against cerebral hyperperfusion during the large arterial pressure surges that characterize this sleep state. We tested this hypothesis using a newly developed model to continuously record SNA in the superior cervical ganglion (SCG) before, during, and after arterial pressure surges occurring during REM in spontaneously sleeping lambs. Arterial pressure (AP), intracranial pressure (ICP), cerebral blood flow (CBF), cerebral vascular resistance [CVR = (AP − ICP)/CBF], and SNA from the SCG were recorded in lambs ( n = 5) undergoing spontaneous sleep-wake cycles. In REM sleep, CBF was greatest (REM > QW = NREM, P < 0.05) and CVR was least (REM < QW = NREM, P < 0.05). SNA in the SCG did not change from QW to NREM sleep but increased during tonic REM sleep, with a further increase during phasic REM sleep (phasic REM > tonic REM > QW = NREM, P < 0.05). Coherent averaging revealed that SNA increases preceded AP surges in phasic REM sleep by 12 s ( P < 0.05). We report the first recordings of cerebral SNA during natural sleep-wake cycles. SNA increases markedly during tonic REM sleep, and further in phasic REM sleep. As SNA increases precede AP surges, they may serve to protect the brain against potentially damaging intravascular pressure changes or hyperperfusion in REM sleep.
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Levine BD, Zhang R. Comments on Point:Counterpoint: Sympathetic activity does/does not influence cerebral blood flow. J Appl Physiol (1985) 2008; 105:1373. [DOI: 10.1152/japplphysiol.zdg-8199.pcpcomm.2008] [Citation(s) in RCA: 19] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/22/2022] Open
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Kulik T, Kusano Y, Aronhime S, Sandler AL, Winn HR. Regulation of cerebral vasculature in normal and ischemic brain. Neuropharmacology 2008; 55:281-8. [PMID: 18541276 PMCID: PMC2896303 DOI: 10.1016/j.neuropharm.2008.04.017] [Citation(s) in RCA: 95] [Impact Index Per Article: 5.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/27/2007] [Revised: 04/19/2008] [Accepted: 04/21/2008] [Indexed: 01/07/2023]
Abstract
We outline the mechanisms currently thought to be responsible for controlling cerebral blood flow (CBF) in the physiologic state and during ischemia, focusing on the arterial pial and penetrating microcirculation. Initially, we categorize the cerebral circulation and then review the vascular anatomy. We draw attention to a number of unique features of the cerebral vasculature, which are relevant to the microcirculatory response during ischemia: arterial histology, species differences, collateral flow, the venous drainage, the blood-brain barrier, astrocytes and vascular nerves. The physiology of the arterial microcirculation is then assessed. Lastly, we review the changes during ischemia which impact on the microcirculation. Further understanding of the normal cerebrovascular anatomy and physiology as well as the pathophysiology of ischemia will allow the rational development of a pharmacologic therapy for human stroke and brain injury.
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Affiliation(s)
- Tobias Kulik
- Department of Neuroscience, Mount Sinai School of Medicine, New York, NY 10029, USA
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Cassaglia PA, Griffiths RI, Walker AM. Sympathetic nerve activity in the superior cervical ganglia increases in response to imposed increases in arterial pressure. Am J Physiol Regul Integr Comp Physiol 2008; 294:R1255-61. [PMID: 18216142 DOI: 10.1152/ajpregu.00332.2007] [Citation(s) in RCA: 112] [Impact Index Per Article: 6.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/22/2022]
Abstract
Sympathetic vasoconstriction of cerebral vessels has been proposed to be a protective mechanism for the brain, limiting cerebral perfusion and microcirculatory pressure during transient increases in arterial pressure. To furnish direct neural evidence for this proposition, we aimed to develop a method for recording cerebral sympathetic nerve activity (SNA) from the superior cervical ganglion (SCG). We hypothesized that SNA recorded from the SCG increases during imposed hypertension, but not during hypotension. Lambs (n = 11) were anesthetized (alpha-chloralose, 20 mg.kg(-1).h(-1)) and ventilated. SNA was measured using 25-microm tungsten microelectrodes inserted into the SCG. Arterial blood pressure (AP) was pharmacologically raised (adrenaline, phenylephrine, or ANG II, 1-50 microg/kg iv), mechanically raised (intravascular balloon in the thoracic aorta), or lowered (sodium nitroprusside, 1-50 microg/kg iv). In response to adrenaline (n = 10), mean AP increased 135 +/- 10% from baseline (mean +/- SE), and the RMS value of SNA (Square Root of the Mean of the Squares, SNA(RMS)) increased 255 +/- 120%. In response to mechanically induced hypertension, mean AP increased 43 +/- 3%, and SNA(RMS) increased 53 +/- 13%. Generally, (9 of 10 animals), SNA(RMS) did not increase, as AP was lowered with sodium nitroprusside. Using a new model for direct recording of cerebral SNA from the SCG, we have demonstrated that SNA increases in response to large induced rises, but not falls, in AP. These findings furnish direct support for the proposed protective role for sympathetic nerves in the cerebral circulation.
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Affiliation(s)
- Priscila A Cassaglia
- Ritchie Centre for Baby Health Research, Monash Institute of Medical Research, Monash University, Clayton, Melbourne, VIC 3168, Australia
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Foster GE, Hanly PJ, Ostrowski M, Poulin MJ. Effects of continuous positive airway pressure on cerebral vascular response to hypoxia in patients with obstructive sleep apnea. Am J Respir Crit Care Med 2007; 175:720-5. [PMID: 17218618 DOI: 10.1164/rccm.200609-1271oc] [Citation(s) in RCA: 67] [Impact Index Per Article: 3.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/18/2023] Open
Abstract
RATIONALE The mechanism leading to increased risk of stroke in patients with obstructive sleep apnea (OSA) is unknown. It may occur through alteration in the regulation of cerebral blood flow, reflected in part by the response of the cerebral vasculature to hypoxia. We hypothesized that the cerebrovascular response to hypoxia is reduced in patients with OSA. OBJECTIVE To determine the cerebral blood flow response to hypoxia in patients with OSA. METHODS The cerebral blood flow response to 20 minutes of isocapnic hypoxia was measured in eight male patients with OSA before and after 4 to 6 weeks of continuous positive airway pressure (CPAP) therapy and in 10 matched healthy control subjects. MEASUREMENTS AND MAIN RESULTS The cerebral blood flow response to hypoxia was significantly lower in patients with OSA compared with control subjects (0.56 +/- 0.10 vs. 0.97 +/- 0.09% [mean +/- SE] change in blood flow velocity per % desaturation; p=0.007). After CPAP therapy, the cerebral blood flow response to hypoxia was similar between patients with OSA and control subjects (1.08 +/- 0.15 vs. 0.92 +/- 0.13% change in blood flow velocity per % desaturation; p=0.4). Moderately strong correlations were found between the cerebral blood flow response to hypoxia and the apnea-hypopnea index (r=-0.57; p=0.04) and nocturnal oxyhemoglobin saturation (r=0.48; p=0.01). CONCLUSIONS The cerebral blood flow response to hypoxia is significantly reduced in patients with OSA. Treatment of OSA with CPAP increases the cerebral blood flow response to hypoxia to normal levels. An attenuated cerebrovascular response to hypoxia in patients with OSA may contribute to their elevated risk of stroke.
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Affiliation(s)
- Glen E Foster
- Department of Physiology and Biophysics, Faculty of Medicine, University of Calgary, Calgary, AB T2N 4N1, Canada
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Van Lieshout JJ, Wieling W, Karemaker JM, Secher NH. Syncope, cerebral perfusion, and oxygenation. J Appl Physiol (1985) 2003; 94:833-48. [PMID: 12571122 DOI: 10.1152/japplphysiol.00260.2002] [Citation(s) in RCA: 266] [Impact Index Per Article: 12.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/22/2022] Open
Abstract
During standing, both the position of the cerebral circulation and the reductions in mean arterial pressure (MAP) and cardiac output challenge cerebral autoregulatory (CA) mechanisms. Syncope is most often associated with the upright position and can be provoked by any condition that jeopardizes cerebral blood flow (CBF) and regional cerebral tissue oxygenation (cO(2)Hb). Reflex (vasovagal) responses, cardiac arrhythmias, and autonomic failure are common causes. An important defense against a critical reduction in the central blood volume is that of muscle activity ("the muscle pump"), and if it is not applied even normal humans faint. Continuous tracking of CBF by transcranial Doppler-determined cerebral blood velocity (V(mean)) and near-infrared spectroscopy-determined cO(2)Hb contribute to understanding the cerebrovascular adjustments to postural stress; e.g., MAP does not necessarily reflect the cerebrovascular phenomena associated with (pre)syncope. CA may be interpreted as a frequency-dependent phenomenon with attenuated transfer of oscillations in MAP to V(mean) at low frequencies. The clinical implication is that CA does not respond to rapid changes in MAP; e.g., there is a transient fall in V(mean) on standing up and therefore a feeling of lightheadedness that even healthy humans sometimes experience. In subjects with recurrent vasovagal syncope, dynamic CA seems not different from that of healthy controls even during the last minutes before the syncope. Redistribution of cardiac output may affect cerebral perfusion by increased cerebral vascular resistance, supporting the view that cerebral perfusion depends on arterial inflow pressure provided that there is a sufficient cardiac output.
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Affiliation(s)
- Johannes J Van Lieshout
- Cardiovascular Research Institute Amsterdam and Departments of Medicine and Physiology, Academic Medical Center, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands.
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Tantucci C, Bottini P, Fiorani C, Dottorini ML, Santeusanio F, Provinciali L, Sorbini CA, Casucci G. Cerebrovascular reactivity and hypercapnic respiratory drive in diabetic autonomic neuropathy. J Appl Physiol (1985) 2001; 90:889-96. [PMID: 11181597 DOI: 10.1152/jappl.2001.90.3.889] [Citation(s) in RCA: 40] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/22/2022] Open
Abstract
Because abnormalities in cerebrovascular reactivity (CVR) in subjects with long-term diabetes could partly be ascribed to autonomic neuropathy and related to central chemosensitivity, CVR and the respiratory drive output during progressive hypercapnia were studied in 15 diabetic patients without (DAN-) and 30 with autonomic neuropathy (DAN+), of whom 15 had postural hypotension (PH) (DAN+PH+) and 15 did not (DAN+PH-), and in 15 control (C) subjects. During CO(2) rebreathing, changes in occlusion pressure and minute ventilation were assessed, and seven subjects in each group had simultaneous measurements of the middle cerebral artery mean blood velocity (MCAV) by transcranial Doppler. The respiratory output to CO(2) was greater in DAN+PH+ than in DAN+PH- and DAN- (P < 0.01), whereas a reduced chemosensitivity was found in DAN+PH- (P < 0.05 vs. C). MCAV increased linearly with the end-tidal PCO(2) (PET(CO(2))) in DAN+PH- but less than in C and DAN- (P < 0.01). In contrast, DAN+PH+ showed an exponential increment in MCAV with PET(CO(2)) mainly >55 Torr. Thus CVR was lower in DAN+ than in C at PET(CO(2)) <55 Torr (P < 0.01), whereas it was greater in DAN+PH+ than in DAN+PH- (P < 0.01) and DAN- (P < 0.05) at PET(CO(2)) >55 Torr. CVR and occlusion pressure during hypercapnia were correlated only in DAN+ (r = 0.91, P < 0.001). We conclude that, in diabetic patients with autonomic neuropathy, CVR to CO(2) is reduced or increased according to the severity of dysautonomy and intensity of stimulus and appears to modulate the hypercapnic respiratory drive.
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Affiliation(s)
- C Tantucci
- Semeiotica e Metodologia Medica, University of Ancona, 60020 Ancona, Italy
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Sakas DE, Moskowitz MA, Wei EP, Kontos HA, Kano M, Ogilvy CS. Trigeminovascular fibers increase blood flow in cortical gray matter by axon reflex-like mechanisms during acute severe hypertension or seizures. Proc Natl Acad Sci U S A 1989; 86:1401-5. [PMID: 2919186 PMCID: PMC286699 DOI: 10.1073/pnas.86.4.1401] [Citation(s) in RCA: 69] [Impact Index Per Article: 1.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/03/2023] Open
Abstract
Cerebral blood flow was measured and compared in 10 symmetrical brain regions following unilateral trigeminal ganglionectomy (n = 13), sham operation (n = 6), or trigeminal root section (rhizotomy) (n = 8) in cats. Multiple determinations were obtained in anesthetized and paralyzed animals using radiolabeled microspheres during (i) normocapnia-normotension, (ii) hypercapnia (5% CO2/95% room air), (iii) angiotensin-induced acute severe hypertension (190 greater than mean arterial blood pressure less than 210 mmHg), or (iv) bicuculline-induced seizures. Flow was symmetrical in all brain regions at rest and during increases induced by hypercapnia in the three groups. During severe hypertension or seizures, marked elevations developed bilaterally (approximately 93% and approximately 130%, respectively). In ganglionectomized animals, increases due to hypertension or seizures were attenuated by 28-32% on the denervated side within cortical gray matter regions corresponding to the anterior, middle, and posterior cerebral arteries. Flow was symmetrical within all brain regions in sham-operated animals and in the rhizotomy group, despite comparable increases in regional cerebral blood flow induced by angiotensin. Hence, the trigeminal nerve mediates blood flow adaptations during severe hypertension and seizures. Furthermore, since trigeminal cell bodies and peripheral axons are destroyed or degenerate following ganglionectomy but not following rhizotomy, local "axon reflex-like" mechanisms mediate these increases in cerebral blood flow.
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Affiliation(s)
- D E Sakas
- Department of Surgery, Harvard Medical School, Massachusetts General Hospital, Boston 02114
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Busija DW, Heistad DD. Effects of activation of sympathetic nerves on cerebral blood flow during hypercapnia in cats and rabbits. J Physiol 1984; 347:35-45. [PMID: 6423816 PMCID: PMC1199432 DOI: 10.1113/jphysiol.1984.sp015051] [Citation(s) in RCA: 43] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/20/2023] Open
Abstract
Effects of unilateral and bilateral activation of sympathetic nerves on cerebral blood flow (c.b.f.) and cerebrovascular resistance (c.v.r.) during hypercapnia were compared in anaesthetized cats and awake rabbits. Sympathetic nerves supplying cerebral vessels were sectioned on one or both sides in anaesthetized cats and unanaesthetized rabbits. Cerebral blood flow was measured with 15 micron radioactive microspheres. In cats, c.b.f. was greater than 110 ml/min per 100 g during hypercapnia (PCO2 greater than 65 mmHg). Unilateral section of sympathetic nerves did not change c.b.f. or c.v.r. but unilateral electrical stimulation decreased c.b.f. by 12 +/- 3% and increased c.v.r. by 15 +/- 4%. Bilateral section of sympathetic nerves decreased c.v.r. by 21 +/- 7% (P less than 0.005, compared with unilateral section) and electrical stimulation increased c.v.r. by 66 +/- 16% (P less than 0.005, compared with unilateral stimulation). In awake rabbits, c.b.f. was greater than 110 ml/min per 100 g during hypercapnia (PCO2 greater than 50 mmHg). Unilateral sympathetic denervation did not change c.v.r. but bilateral denervation decreased it by 18 +/- 8% (P less than 0.08, compared with unilateral section; P less than 0.03, compared with intact nerves). Thus, reflex activation of sympathetic nerves, as well as electrical stimulation, increases c.v.r. during hypercapnia. In addition, effects of bilateral stimulation or denervation of sympathetic nerves are greater than unilateral effects.
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Crystal GJ, Downey HF, Adkins TP, Bashour FA. Regional blood flow in canine brain during nicotine infusion: effect of autonomic blocking drugs. Stroke 1983; 14:941-7. [PMID: 6140781 DOI: 10.1161/01.str.14.6.941] [Citation(s) in RCA: 10] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/18/2023]
Abstract
Radioactive microspheres (15 mu) were used to measure regional cerebral blood flow during intravenous infusion of nicotine (36 micrograms/kg/min) in anesthetized, open chest dogs. Experiments were conducted with uncontrolled mean aortic pressure and intact autonomic receptors (Series I; n = 9), and in four groups of dogs with mean aortic pressure held constant (Series II); 1) with intact autonomic receptors (n = 6), 2) after beta adrenergic blockade (n = 8), 3) after alpha and beta adrenergic blockade (n = 6), 4) after alpha and beta adrenergic and cholinergic blockade (n = 4). In Series I, nicotine raised mean aortic pressure (+ 72%) and increased flow in cerebral cortex (+ 67%), cerebellum (+ 38%), pons (+ 46%), medulla (+ 39%), and spinal cord (+ 48%). In all regions, but cortex, increases in vascular resistance limited nicotine-induced increases in flow. In Series II, nicotine changed flow only in cortex. Without blockade, nicotine increased cortical flow (+ 38%); but beta blockade abolished this increase in flow. After alpha and beta blockade nicotine again raised cortical flow (+ 29%), and additional cholinergic blockade had no effect on this response. It is concluded that nicotine causes predominant beta receptor mediated vasodilation in cerebral cortex, although it also activates alpha (vasoconstrictor) receptors and a non-adrenergic, non-cholinergic vasodilator mechanism in this region of brain.
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Igloffstein J, Laas R. Cerebral infarction due to carotid occlusion and carbon monoxide exposure. II. Influence of preganglionic cervical sympathectomy. J Neurol Neurosurg Psychiatry 1983; 46:768-73. [PMID: 6886721 PMCID: PMC1027532 DOI: 10.1136/jnnp.46.8.768] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/22/2023]
Abstract
Unilateral cerebral infarcts were produced in the rat by ligation of one common carotid artery and subsequent exposure to carbon monoxide. The incidence and extension of brain infarcts was increased in animals with additional ipsilateral cervical preganglionic sympathectomy. Sympathectomy did not affect markedly the respiration and systemic circulation. The effect of sympathectomy was attributed to a cutaneous vasodilation, leading to an extracranial steal phenomenon.
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Abstract
1 The role of the sympathetic innervation of cerebral arteries remains controversial. Therefore, the functional activity of the adrenergic innervation of the rabbit basilar artery was characterized and compared to that of a peripheral artery, the ear artery. 2 Both the ear artery and basilar artery have similar endogenous noradrenaline (NA) contents but accumulation of [3H]-NA was considerably greater in the basilar artery. 3 Studies of tritium efflux after loading with [3H]-NA demonstrated a considerable non-neuronal component since neither guanethidine nor tetrodotoxin completely blocked tritium efflux during nerve stimulation. Pretreatment with blockers of uptake2 did not eliminate this problem. 4 Comparison of methods for estimating the functional activity of adrenergic nerves showed that, for the vessels studied, NA content and [3H]-NA accumulation gave markedly different answers. Fractional release of [3H]-NA did not correspond to fractional release of endogenous NA. 5 Adrenergic nerves innervating cerebral arteries are shown to have a high activity relative to a peripheral artery. While cerebrovascular sympathetic innervation may not play an important role in normal circumstances, its influence may be seen in pathological conditions.
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Hayashi S, Miyazaki M, Toda N. Responsiveness to vasoactive agents of cerebral and mesenteric arteries isolated from control and reserpine-treated dogs. Br J Pharmacol 1980; 68:473-8. [PMID: 7052340 PMCID: PMC2044211 DOI: 10.1111/j.1476-5381.1980.tb14561.x] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/23/2023] Open
Abstract
1 Pretreatment of dogs for 20 to 24 h before the start of experiments with reserpine (0.5 mg/kg) depleted noradrenaline from cerebral and mesenteric arteries, the diminution being greater in the latter arteries. 2 Contractile responses of helically-cut strips of cerebral and mesenteric arteries to noradrenaline were unaffected by pretreatment with reserpine. Tyramine-induced contractions of mesenteric arteries were markedly attenuated by reserpine-pretreatment, whereas the contraction of cerebral arteries was not influenced. The contractile response of mesenteric arteries to transmural nerve stimulation or nicotine was abolished by reserpine-pretreatment, but the relaxation induced by nicotine of cerebral arteries contracted with prostaglandin F2 alpha was not affected. Pretreatment with reserpine attenuated the contractions of mesenteric arteries induced by angiotensin II, but did not alter the response of cerebral arteries to 5-hydroxytryptamine. 3 In prostaglandin-contracted cerebral and mesenteric arterial strips, relaxant effects of acetylcholine, isoprenaline and K+ were not significantly influenced by reserpine-pretreatment. 4 It appears that tyramine and nicotine do not release noradrenaline from dog cerebral arteries in amounts sufficient to cause significant contractions. Attenuation of the response to angiotensin II by pretreatment with reserpine is not the result of depletion of noradrenaline from the mesenteric arterial wall but may be due to interference with the mechanism specific to actions of angiotensin II.
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