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World J Cardiol. Jun 26, 2017; 9(6): 508-520
Published online Jun 26, 2017. doi: 10.4330/wjc.v9.i6.508
Influence of cardiac nerve status on cardiovascular regulation and cardioprotection
John G Kingma, Denys Simard, Jacques R Rouleau
John G Kingma, Jacques R Rouleau, Department of Medicine, Faculty of Medicine, Laval University, Québec, QC G1V 4G5, Canada
Denys Simard, Centre de Recherche de l’Institut de Cardiologie et de Pneumologie de Québec - Université Laval, Québec, QC G1V 4G5, Canada
Author contributions: Kingma JG wrote the initial draft and contributed to conception and design as well as interpretation of data; Simard D performed bibliographic searches and contributed to editorial review, analysis of data and intellectual content; Rouleau JR contributed to critical editorial review and intellectual content.
Conflict-of-interest statement: The authors declare no conflict of interest with regard to research, authorship or publication for this article.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: John G Kingma, PhD, Department of Medicine, Faculty of Medicine, Laval University, 2725 chemin Ste-Foy, Ste-Foy, Québec, QC G1V 4G5, Canada. john.kingma@fmed.ulaval.ca
Telephone: +1-418-6568711-5440
Received: January 28, 2017
Peer-review started: February 10, 2017
First decision: March 6, 2017
Revised: March 22, 2017
Accepted: April 23, 2017
Article in press: April 24, 2017
Published online: June 26, 2017
Processing time: 148 Days and 20.5 Hours
Abstract

Neural elements of the intrinsic cardiac nervous system transduce sensory inputs from the heart, blood vessels and other organs to ensure adequate cardiac function on a beat-to-beat basis. This inter-organ crosstalk is critical for normal function of the heart and other organs; derangements within the nervous system hierarchy contribute to pathogenesis of organ dysfunction. The role of intact cardiac nerves in development of, as well as protection against, ischemic injury is of current interest since it may involve recruitment of intrinsic cardiac ganglia. For instance, ischemic conditioning, a novel protection strategy against organ injury, and in particular remote conditioning, is likely mediated by activation of neural pathways or by endogenous cytoprotective blood-borne substances that stimulate different signalling pathways. This discovery reinforces the concept that inter-organ communication, and maintenance thereof, is key. As such, greater understanding of mechanisms and elucidation of treatment strategies is imperative to improve clinical outcomes particularly in patients with comorbidities. For instance, autonomic imbalance between sympathetic and parasympathetic nervous system regulation can initiate cardiovascular autonomic neuropathy that compromises cardiac stability and function. Neuromodulation therapies that directly target the intrinsic cardiac nervous system or other elements of the nervous system hierarchy are currently being investigated for treatment of different maladies in animal and human studies.

Keywords: Intrinsic cardiac nervous system; Myocardial ischemia; Ischemic conditioning; Autonomic neuropathy; Coronary blood flow regulation

Core tip: Neural elements within the intrinsic cardiac nervous system are known to transduce sensory inputs from the heart, blood vessels and surrounding organs to ensure beat-to-beat regulation of cardiac function. Development of autonomic neurophathies in patients with comorbidities compromises clinical outcomes. Myocardial ischemia also significantly affects cardiocytes as well as cardiac neurons; post-ischemic remodelling might affect neuronal function and thereby contribute to cardiac instability. Different protection strategies including ischemic conditioning and neuromodulation interventions that limit neural injury and help maintain cardiovascular function are the subject of ongoing investigations.