• Ischaemic neuromyelomyopathy
• Kippfenster syndrome
• crush injury
• window entrapment

• Animals
• Cats
• Female
• Male
• Cat Diseases/pathology
• Prognosis
• Retrospective Studies
• Neuromuscular Diseases/veterinary

• Autophagy
• Ketamine
• Langendorff
• Myocardial ischemia-reperfusion injury
• Quercetin
• Remote ischemic preconditioning

The incidence of internal hernias has recently increased in concordance with the popularization of laparoscopic surgery. Of particular concern are internal hernias occurring in Petersen's space, a space that is surgically created after treatment for gastric cancer and obesity. These hernias cause devastating sequelae, such as massive intestinal necrosis, fatal Roux limb necrosis, and superior mesenteric vein thrombus. In addition, protein-losing enteropathy (PLE) is a rare syndrome involving gastrointestinal protein loss, although its relationship with internal Petersen’s hernias remains unknown.

A 75-year-old man with a history of laparotomy for early gastric cancer developed Petersen's hernia 1 year and 5 mo after surgery. He was successfully treated by reducing the incarcerated small intestine and closure of Petersen’s defect without resection of the small intestine. Approximately 3 mo after his surgery for Petersen’s hernia, he developed bilateral leg edema and hypoalbuminemia. He was diagnosed with PLE with an alpha-1 antitrypsin clearance of 733 mL/24 h. Double-balloon enteroscopy revealed extensive jejunal ulceration as the etiology, and it facilitated minimum bowel resection. Pathological analysis showed extensive jejunal ulceration and collagen hyperplasia with nonspecific inflammation of all layers without lymphangiectasia, lymphoma, or vascular abnormalities. His postoperative course was unremarkable, and his bilateral leg edema and hypoalbuminemia improved after 1 mo. There was no relapse over the 5-year follow-up period.

PLE and extensive jejunal ulceration may occur after Petersen's hernia. Double-balloon enteroscopy helps identify and resect these lesions.

• Internal hernia
• Ulcer
• Protein-losing enteropathy
• Double-balloon enteroscopy
• Ischemia-reperfusion injury
• Case report

To evaluate if the perconditioning affects the antioxidant capacity in mesenteric ischemia and reperfusion injury.

Twenty-one Wistar rats were assigned into three groups, as follows: Sham, IR and rPER. The animals were subjected to mesenteric ischemia for 30 min. rPER consisted of three cycles of 5-min hindlimb ischemia followed by 5 min hindlimb perfusion at the same time to mesenteric ischemic period. After 5 minutes, blood and 5 cm of terminal ileum were harvested for thiobarbituric acid reactive substances (TBARS) and Trolox equivalent antioxidant capacity (TEAC) measurement.

rPER technique was able to reduce intestinal tissue TBARS levels (p<0.0001), but no statistic difference was observed in blood levels between groups, although it was verified similar results in rPER and Sham group. rPER technique also enhanced TEAC levels in both blood (p = 0.0314) and intestinal tissue (p = 0.0139), compared to IR group.

rPER appears as the most promising technique to avoid IR injury. This technique reduced TBARS levels in blood and intestinal tissue and promoted the maintenance of antioxidant defense in mesenteric acute injury.

• Humans
• Male
• Female
• Oxygen/metabolism
• Critical Illness
• Retrospective Studies
• Middle Aged
• Aged
• Ischemia/etiology
• Case-Control Studies
• Intestines/blood supply
• Hemoglobins/metabolism
• Hemoglobins/analysis
• Oxygen Saturation
• Lactic Acid/blood
• Vascular Resistance

• Klaus Tschira Stiftung

• Desloratadine
• ischemia
• rat
• renal
• reperfusion

• ischemia-reperfusion
• lycopene
• ovary
• rat

• Animals
• Anti-Inflammatory Agents
• Antioxidants
• Apoptosis/drug effects
• Female
• Injections, Intraperitoneal
• Ischemia/drug therapy
• Ischemia/etiology
• Ischemia/pathology
• Ischemia/prevention & control
• Lycopene/administration & dosage
• Lycopene/pharmacology
• Malondialdehyde/metabolism
• NF-kappa B/metabolism
• Ovarian Torsion/complications
• Ovary/blood supply
• Ovary/metabolism
• Oxidative Stress/physiology
• Phosphorylation
• Rats, Wistar
• Reperfusion Injury/complications
• Rats

The present study aimed to explore the protective effects of extracorporeal membrane oxygenation (ECMO) on intestinal mucosal injury following cardiopulmonary resuscitation (CPR), and to assess the potential mechanisms involved. A total of 24 healthy adult domestic pigs were selected as the study subjects. A ventricular fibrillation model was induced through programmed electric stimulation. Subsequently, the animals were randomly divided into conventional CPR and CPR+ECMO groups (n=12 per group). The mortality and hemodynamic parameters of the two groups were compared. The expression levels of inflammatory cytokines in the serum and intestinal mucosa were detected by ELISAs. The intestinal mucosa was subjected to hematoxylin and eosin, and immunohistochemical staining, followed by electron microscopy, to assess the degree of apoptosis and necrosis. The animals in both groups recovered from the programmed ventricular fibrillation. In the CPR group, two animals died at 2 h and two more animals died a further 2 h later, resulting in a 33.3% mortality rate, whereas no cases of mortality were observed in the CPR+ECMO group. Compared with the animals in the CPR group, the hemodynamic parameters of the animals in the CPR+ECMO group revealed significantly improved outcomes. Multiple inflammatory factors (tumor necrosis factor α, interleukin-1 and interleukin-6), myeloperoxidase and malondialdehyde levels were decreased, whereas Na/Ca-ATPase and superoxide dismutase levels were elevated in the intestinal mucosa of animals in the CPR+ECMO group compared with those in the CPR group. Additionally, pathological staining demonstrated that the intestinal mucosa tissue in the CPR+ECMO group exhibited less apoptosis, necrosis and inflammatory cell infiltration, which was further supported by a decrease in Bax expression and an increase in Bcl-2 expression. Overall, ECMO after CPR reduced the intestinal mucosal barrier injury after spontaneous circulation recovery, and the mechanism involved decreased inflammation and apoptosis.

• cardiac arrest
• cardiopulmonary resuscitation
• extracorporeal membrane oxygenation
• intestinal mucosal barrier

• femoropopliteal bypass
• ischemia-reperfusion
• peripheral artery disease
• vesicles and bullae

Small renal masses have been diagnosed increasingly in recent decades, allowing surgical treatment by partial nephrectomy. This treatment option is associated with better renal function preservation, in comparison with radical nephrectomy. However, for obtaining a bloodless field during surgery, occlusion of renal artery and veins is often required, which results in transitory ischemia. The renal ischemia-reperfusion injury is associated with increased reactive oxygen species production leading to renal tissue damage. Thus, the use of antioxidants has been advocated in the partial nephrectomy perioperative period. Several antioxidants were investigated in regard to renal ischemia-reperfusion injury. The present manuscript aims to present the literature on the most commonly studied antioxidants used during partial nephrectomy. The results of experimental and clinical studies using antioxidants during partial nephrectomy are reported. Further, alimentary sources of some antioxidants are presented, stimulating future studies focusing on perioperative antioxidant-rich diets.

• Animals
• Deoxyribonuclease I/pharmacology
• Disease Models, Animal
• Extracellular Traps/drug effects
• Inflammation/drug therapy
• Intestines/drug effects
• Kidney/drug effects
• Male
• Myocardium/pathology
• Neutrophils/drug effects
• Protective Agents/pharmacology
• Rats
• Rats, Sprague-Dawley
• Reperfusion Injury/drug therapy

• 81770532 National Natural Science Foundation of China (National Science Foundation of China)
• the Military Logistics Research Project (grant No. CNJ16C010), Jiangsu Province Medical Foundation for Youth Talents (grant No. QNRC2016901).

• gut ischemia-reperfusion
• inflammation
• inhibitor
• organ injury
• ubiquitination

• Toll-like receptors
• intestinal ischemia reperfusion injury
• microbiome
• oxidative stress

To investigate viability assessment of segmental small bowel ischemia/reperfusion in a porcine model.

In 15 pigs, five or six 30-cm segments of jejunum were simultaneously made ischemic by clamping the mesenteric arteries and veins for 1 to 16 h. Reperfusion was initiated after different intervals of ischemia (1-8 h) and subsequently monitored for 5-15 h. The intestinal segments were regularly photographed and assessed visually and by palpation. Intraluminal lactate and glycerol concentrations were measured by microdialysis, and samples were collected for light microscopy and transmission electron microscopy. The histological changes were described and graded.

Using light microscopy, the jejunum was considered as viable until 6 h of ischemia, while with transmission electron microscopy the ischemic muscularis propria was considered viable until 5 h of ischemia. However, following ≥ 1 h of reperfusion, only segments that had been ischemic for ≤ 3 h appeared viable, suggesting a possible upper limit for viability in the porcine mesenteric occlusion model. Although intraluminal microdialysis allowed us to closely monitor the onset and duration of ischemia and the onset of reperfusion, we were unable to find sufficient level of association between tissue viability and metabolic markers to conclude that microdialysis is clinically relevant for viability assessment. Evaluation of color and motility appears to be poor indicators of intestinal viability.

Three hours of total ischemia of the small bowel followed by reperfusion appears to be the upper limit for viability in this porcine mesenteric ischemia model.

• Viability
• Histology
• Reperfusion
• Ischemia
• Microdialysis
• Jejunum
• Porcine model

• Animals
• Color
• Female
• Gastrointestinal Motility
• Intestinal Mucosa/blood supply
• Intestinal Mucosa/diagnostic imaging
• Intestinal Mucosa/pathology
• Intestinal Mucosa/ultrastructure
• Jejunum/blood supply
• Jejunum/diagnostic imaging
• Jejunum/pathology
• Jejunum/ultrastructure
• Male
• Mesenteric Vascular Occlusion/complications
• Microdialysis
• Microscopy, Electron, Transmission
• Photography
• Reperfusion Injury/diagnostic imaging
• Reperfusion Injury/etiology
• Reperfusion Injury/pathology
• Sus scrofa
• Swine
• Time Factors
• Tissue Survival

• Bacterial translocation
• NO toxicity
• antioxidants
• free radicals
• intestinal ischemia
• oxidative stress
• reactive oxygen species
• reperfusion injury

• Abdominal compartment syndrome
• Blunt
• Lower extremity trauma
• Penetrating
• Vascular injury

• Adult
• Female
• Florida/epidemiology
• Humans
• Injury Severity Score
• Intra-Abdominal Hypertension/diagnosis
• Intra-Abdominal Hypertension/etiology
• Intra-Abdominal Hypertension/mortality
• Intra-Abdominal Hypertension/prevention & control
• Lower Extremity/blood supply
• Lower Extremity/injuries
• Male
• Middle Aged
• Outcome and Process Assessment, Health Care
• Retrospective Studies
• Trauma Centers/statistics & numerical data
• Vascular Surgical Procedures/methods
• Vascular System Injuries/complications
• Vascular System Injuries/diagnosis
• Vascular System Injuries/surgery
• Wounds, Penetrating/complications
• Wounds, Penetrating/diagnosis
• Wounds, Penetrating/surgery

Some publications have demonstrated the presence of lung reperfusion injury in mesenteric ischemia and reperfusion (I/R), but under to diverse methods. Postconditioning has been recognized as effective in preventing reperfusion injury in various organs and tissues. However, its effectiveness has not been evaluated in the prevention of lung reperfusion injury after mesenteric ischemia and reperfusion.

To evaluate the presence of pulmonary reperfusion injury and the protective effect of ischemic postconditioning on lung parenchyma in rats submitted to mesenteric ischemia and reperfusion.

Thirty Wistar rats were distributed into three groups: group A (10 rats), which was held mesenteric ischemia (30 minutes) and reperfusion (60 minutes); group B (10 rats), ischemia and reperfusion, interspersed by postconditioning with two alternating cycles of reperfusion and reocclusion, for two minutes each; and group C (10 rats), ischemia and reperfusion interleaved by postconditioning with four alternating cycles of reperfusion and reocclusion of 30 seconds each. Finally, it was resected the upper lung lobe for histological analysis.

There were mild lung lesions (grade 1) in all samples. There was no statistical difference between groups 1 and 2 (P>0.05).

The mesenteric ischemia and reperfusion in rats for thirty and sixty minutes, respectively, caused mild reperfusion injury in lung. Postconditioning was not able to minimize the remote reperfusion injury and there was no difference comparing two cycles of two minutes with four cycles of 30 seconds.

Brain stroke is a leading cause of death without effective treatment. Feronia limonia have potent antioxidant activity and can be proved as neuroprotective against ischemia-reperfusion induced brain injury.

We studied the effect of methanolic extract of F. limonia fruit (250 mg/kg, 500 mg/kg body weight, p.o.) and Vitamin E as reference standard drug on 30 min induced ischemia, followed by reperfusion by testing the neurobehavioral tests such as neurodeficit score, rota rod test, hanging wire test, beam walk test and elevated plus maze. The biochemical parameters, which were measured in animals brain were catalase, superoxide dismutase (SOD), malondialdehyde and nitric oxide in control and treated rats.

The methanolic extract of F. limonia fruit (250 mg/kg, 500 mg/kg body weight, p.o.) treated groups showed a statistically significant improvement in the neurobehavioral parameters such as motor performance (neurological status, significant increase in grasping ability, forelimb strength improvement in balance and co-ordination). The biochemical parameters in the brains of rats showed a significant reduction in the total nitrite (P < 0.01) and lipid peroxidation (P < 0.01), also a significant enhanced activity of enzymatic antioxidants such as catalase (P < 0.01) and SOD (P < 0.05).

These observations suggest the neuroprotective and antioxidant activity of F. limonia and Vitamin E on ischemia reperfusion induced brain injury and may require further evaluation.

• Brain ischemia-reperfusion
• Feronia limonia
• neuroprotection
• oxidative stress

Ischemic postconditioning has been recognized as effective in the prevention of reperfusion injury in situations of ischemia and reperfusion in various organs and tissues. However, it remains unclear what would be the best way to accomplish it, since studies show great variation in the method of their application.

To assess the protective effect of ischemic postconditioning on ischemia and reperfusion in rats undergoing five alternating cycles of reperfusion and ischemia of 30 seconds each one.

We studied 25 Wistar rats distributed in three groups: group A (10 rats), which underwent mesenteric ischemia (30 minutes) and reperfusion (60 minutes); Group B (10 rats), undergoing ischemia (30 minutes) and reperfusion (60 minutes), intercalated by postconditioning (5 alternating cycles of reperfusion and ischemia of 30 seconds each one); and group C - SHAM (5 rats), undergoing only laparotomy and manipulation of mesenteric artery. All animals underwent resection of an ileum segment for histological analysis.

The mean lesions degree according to Chiu et al. were: group A, 2.77, group B, 2.67 and group C, 0.12. There was no difference between groups A and B (P>0.05).

Ischemic postconditioning was not able to minimize or prevent the intestinal tissue injury in rats undergoing ischemia and reperfusion process when used five cycles lasting 30 seconds each one.

Organ injury occurs not only during periods of ischemia but also during reperfusion. It is known that ischemia reperfusion (IR) causes both remote organ and local injuries.

This study evaluated the effects of tramadol on the heart as a remote organ after acute hindlimb IR.

Thirty healthy mature male Wistar rats were allocated randomly into three groups: Group I (sham), Group II (IR), and Group III (IR + tramadol). Ischemia was induced in anesthetized rats by left femoral artery clamping for 3 h, followed by 3 h of reperfusion. Tramadol (20 mg/kg, intravenous) was administered immediately prior to reperfusion. At the end of the reperfusion, animals were euthanized, and hearts were harvested for histological and biochemical examination.

The levels of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were higher in Groups I and III than those in Group II (p < 0.05). In comparison with other groups, tissue malondialdehyde (MDA) levels in Group II were significantly increased (p < 0.05), and this increase was prevented by tramadol. Histopathological changes, including microscopic bleeding, edema, neutrophil infiltration, and necrosis, were scored. The total injuryscore in Group III was significantly decreased (p < 0.05) compared with Group II.

From the histological and biochemical perspectives, treatment with tramadol alleviated the myocardial injuries induced by skeletal muscle IR in this experimental model.

• Ischemia
• reperfusion damage

• animal model
• intestine
• ischemia
• mucosal injury
• reperfusion

• ischemic reperfusion injury
• ischemic preconditioning
• systemic inflammatory response
• intestinal ischemia
• hemocytometry
• superior mesenteric artery occlusion

• Animals
• Biomarkers/blood
• Blood Cell Count
• Blood Cells
• Intestines/blood supply
• Intestines/surgery
• Ischemia/blood
• Ischemic Preconditioning/methods
• Laparotomy/methods
• Male
• Predictive Value of Tests
• Prospective Studies
• Random Allocation
• Rats, Wistar
• Reference Values
• Reperfusion Injury/blood
• Reperfusion Injury/prevention & control
• Reproducibility of Results
• Time Factors

• bacterial translocation
• ischemia/reperfusion
• mucosal barrier dysfunction
• trapidil

Mesenteric ischemia-reperfusion (IR) is associated with impairment of the gut barrier function and the initiation of a proinflammatory cascade with life-threatening results. Therefore methods directed to ameliorate IR injury are of great importance. We aimed at describing the effects of postconditioning (PC) on the alterations of the intestinal mucosal function and the inflammatory response upon mesenteric IR. Methods. Male Wistar rats were gavaged with green fluorescent protein-expressing E. coli suspensions. Animals were randomized into three groups (n = 15), sham-operated, IR-, and PC-groups, and underwent 60 minutes of superior mesenteric artery occlusion, followed by 6 hours of reperfusion. Postconditioning was performed at the onset of reperfusion. Blood and tissue samples were taken at the end of reperfusion, for histological, bacteriological, and plasma examinations. Results. The PC-group presented a more favorable claudin-2, claudin-3, claudin-4, and zonula occludens-1 membrane expression profile, and significantly lower rates of bacterial translocation to distant organs and plasma D-lactate levels compared to the IR-group. Histopathological lesions, plasma I-FABP, IL-6, and TNF-α levels were significantly lower in the PC-group compared to the IR-group. Conclusion. The use of postconditioning improved the integrity of the intestinal mucosal barrier upon mesenteric IR, and thus reduced the incidence of bacterial translocation and development of a systemic inflammatory response.

To evaluate the possible protective effect of pomegranate extract (PE) on rats following renal ischemia–reperfusion (I/R) injury.

Twenty-four Wistar rats were divided into three groups. Sham group underwent laparotomy then waited for 45 minutes without ischemia. I/R group were subjected to left renal ischemia for 45 minutes followed by 60 minutes of reperfusion. I/R + PE group were subjected to the same renal I/R as the I/R group were also given 225 mg/kg PE peroral 30 minutes prior to the ischemia. Malondialdehyde (MDA), total antioxidant capacity (TAC), total oxidant status (TOS), and oxidative stress index (OSI) were determined on the blood samples and kidney tissues. Histopathological analyses were conducted on the kidney tissues.

Serum TAC levels were significantly decreased in I/R group when compared with S group (P = 0.001). Serum MDA levels were increased in I/R group; however, it was not statistically significant. In rat kidney tissues, TOS levels and OSI index were significantly increased after I/R injury, while TAC levels were decreased. In I/R + PE group, PE reversed the negative effects of I/R injury. PE pretreatment was effective in decreasing tubular necrosis score.

PE pretreatment ameliorated the oxidative damage and histopathological changes occurring following renal I/R injury.

• Antioxidant
• ischemia-reperfusion
• kidney
• pomegranate extract
• rat

• HB-EGF
• Hemorrhagic shock
• Intestinal injury
• Ischemia and reperfusion
• Necrotizing enterocolitis

Ischemia associated injury of the myocardium is caused by oxidative damage during reperfusion. Myocardial protection by ischemic preconditioning (IPC) was shown to be mediated by a transient ‘iron-signal’ that leads to the accumulation of apoferritin and sequestration of reactive iron released during the ischemia. Here we identified the source of this ‘iron signal’ and evaluated its role in the mechanisms of cardiac protection by hypoxic preconditioning. Rat hearts were retrogradely perfused and the effect of proteasomal and lysosomal protease inhibitors on ferritin levels were measured. The iron-signal was abolished, ferritin levels were not increased and cardiac protection was diminished by inhibition of the proteasome prior to IPC. Similarly, double amounts of ferritin and better recovery after ex vivo ischemia-and-reperfusion (I/R) were found in hearts from in vivo hypoxia pre-conditioned animals. IPC followed by normoxic perfusion for 30 min (‘delay’) prior to I/R caused a reduced ferritin accumulation at the end of the ischemia phase and reduced protection. Full restoration of the IPC-mediated cardiac protection was achieved by employing lysosomal inhibitors during the ‘delay’. In conclusion, proteasomal protein degradation of iron-proteins causes the generation of the ‘iron-signal’ by IPC, ensuing de-novo apoferritin synthesis and thus, sequestering reactive iron. Lysosomal proteases are involved in subsequent ferritin breakdown as revealed by the use of specific pathway inhibitors during the ‘delay’. We suggest that proteasomal iron-protein degradation is a stress response causing an expeditious cytosolic iron release thus, altering iron homeostasis to protect the myocardium during I/R, while lysosomal ferritin degradation is part of housekeeping iron homeostasis.

Small intestinal ischemia-reperfusion (IR) is a frequent, potentially life threatening phenomenon. There is a lack of non-invasive diagnostic modalities. For many intestinal diseases, visualizing the intestinal mucosa using endoscopy is gold standard. However, limited knowledge exists on small intestinal IR-induced, early mucosal changes. The aims of this study were to investigate endoscopic changes in human jejunum exposed to IR, and to study concordance between endoscopic appearance and histology.

In 23 patients a part of jejunum, to be removed for surgical reasons, was isolated and selectively exposed to ischemia with 0, 30 or 120 minutes of reperfusion. In 3 patients, a videocapsule was inserted in the isolated segment before exposure to IR, to visualize the mucosa. Endoscopic view at several time points was related to histology (Heamatoxylin & Eosin) obtained from 20 patients.

Ischemia was characterized by loss of villous structure, mucosal whitening and appearance of punctate lesions. This was related to appearance of subepithelial spaces and breaches in the epithelial lining in the histological view. Early during reperfusion, the lumen filled with IR-damaged, shed cells and VCE showed mucosal erosions, hemorrhage and intraluminal debris. At 60 minutes of reperfusion, the only remaining signs of IR were loss of villous structure and small erosions, indicating rapid mucosal healing.

This study shows a unique, real-time in vivo endoscopic view of early mucosal changes during IR of the human small intestine. Future studies should evaluate its usefulness in diagnosis of patients suspected of IR.

• Blood Flow Velocity
• Cycloheximide/pharmacology
• Cytokines/metabolism
• E-Selectin/metabolism
• Endothelial Cells/metabolism
• Erythrocytes/cytology
• Gene Expression Regulation
• Hemodynamics
• Human Umbilical Vein Endothelial Cells
• Humans
• Inflammation
• Interleukin-1beta/metabolism
• Models, Biological
• Neutrophils/metabolism
• Protein Synthesis Inhibitors/pharmacology
• Shear Strength
• Stress, Mechanical

• T32 GM145304 NIGMS NIH HHS