scholarly journals Increased mRNA Expression of Endothelial Adhesion Molecules and Proinflammatory Cytokines in the Type 2 Diabetic Heart Following Ischemia/Reperfusion Injury

2007 ◽  
Vol 21 (6) ◽  
Author(s):  
Garrett S. Pacheco ◽  
Corrine E. Walker ◽  
Laura R. La Bonte ◽  
Grace Davis‐Gorman ◽  
Gregory L. Stahl ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Mrna Expression ◽  
Adhesion Molecules ◽  
Proinflammatory Cytokines ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Diabetic Heart ◽  
Endothelial Adhesion Molecules ◽  
Type 2 Diabetic

Hydrogen sulfide attenuates lung ischemia–reperfusion injury through SIRT3-dependent regulation of mitochondrial function in type 2 diabetic rats

Surgery ◽  
2019 ◽  
Vol 165 (5) ◽  
pp. 1014-1026 ◽  
Author(s):  
Tao Jiang ◽  
Yanhong Liu ◽  
Qiuming Meng ◽  
Xiangqi Lv ◽  
Ziyong Yue ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Reperfusion Injury ◽  
Mitochondrial Function ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Diabetic Rats ◽  
Type 2 Diabetic

PPAR-α activation protects the type 2 diabetic myocardium against ischemia-reperfusion injury: involvement of the PI3-Kinase/Akt and NO pathway

2009 ◽  
Vol 296 (3) ◽  
pp. H719-H727 ◽  
Author(s):  
Aliaksandr A. Bulhak ◽  
Christian Jung ◽  
Claes-Göran Östenson ◽  
Jon O. Lundberg ◽  
Per-Ove Sjöquist ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
No Synthase ◽  
Ischemic Myocardium ◽  
No Production ◽  
Gk Rats ◽  
Nitrite Nitrate ◽  
Type 2 Diabetic

Several clinical studies have shown the beneficial cardiovascular effects of fibrates in patients with diabetes and insulin resistance. The ligands of peroxisome proliferator-activated receptor-α (PPAR-α) reduce ischemia-reperfusion injury in nondiabetic animals. We hypothesized that the activation of PPAR-α would exert cardioprotection in type 2 diabetic Goto-Kakizaki (GK) rats, involving mechanisms related to nitric oxide (NO) production via the phosphatidylinositol 3-kinase (PI3K)/Akt pathway. GK rats and age-matched Wistar rats (n ≥ 7) were given either 1) the PPAR-α agonist WY-14643 (WY), 2) dimethyl sulfoxide (DMSO), 3) WY and the NO synthase inhibitor NG-nitro-l-arginine (l-NNA), 4) l-NNA, 5) WY and the PI3K inhibitor wortmannin, or 6) wortmannin alone intravenously before a 35-min period of coronary artery occlusion followed by 2 h of reperfusion. Infarct size (IS), expression of endothelial NO synthase (eNOS), inducible NO synthase, and Akt as well as nitrite/nitrate were determined. The IS was 75 ± 3% and 72 ± 4% of the area at risk in the Wistar and GK DMSO groups, respectively. WY reduced IS to 56 ± 3% in Wistar ( P < 0.05) and to 46 ± 5% in GK rats ( P < 0.001). The addition of either l-NNA or wortmannin reversed the cardioprotective effect of WY in both Wistar (IS, 70 ± 5% and 65 ± 5%, respectively) and GK (IS, 66 ± 4% and 64 ± 4%, P < 0.05, respectively) rats. The expression of eNOS and eNOS Ser1177 in the ischemic myocardium from both strains was increased after WY. The expression of Akt, Akt Ser473, and Akt Thr308 was also increased in the ischemic myocardium from GK rats following WY. Myocardial nitrite/nitrate levels were reduced in GK rats ( P < 0.05). The results suggest that PPAR-α activation protects the type 2 diabetic rat myocardium against ischemia-reperfusion injury via the activation of the PI3K/Akt and NO pathway.

scholarly journals Sevoflurane Reduces Leukocyte and Platelet Adhesion after Ischemia-Reperfusion by Protecting the Endothelial Glycocalyx

2011 ◽  
Vol 115 (3) ◽  
pp. 483-491 ◽  
Author(s):  
Daniel Chappell ◽  
Bernhard Heindl ◽  
Matthias Jacob ◽  
Thorsten Annecke ◽  
Congcong Chen ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Reperfusion Injury ◽  
Adhesion Molecules ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Volatile Anesthetics ◽  
Endothelial Glycocalyx ◽  
Myocardial Infarct Size ◽  
Minimal Alveolar Concentration ◽  
Endothelial Adhesion Molecules

Background Adhesion of polymorphonuclear neutrophils and platelets to the vessel wall contributes to generating ischemia-reperfusion injury. Endothelial adhesion molecules are harbored within the glycocalyx, which covers every healthy vascular endothelium but is deteriorated by ischemia-reperfusion. Pretreating the heart with volatile anesthetics reduces myocardial infarct size and protects against ischemia-reperfusion injury. The authors analyzed a possible protective effect of sevoflurane on the glycocalyx and implications for postischemic cell adhesion. Methods Isolated guinea pig hearts were perfused with crystalloid buffer and subjected to 20 min of global warm ischemia and 10 min of reperfusion. An intracoronary bolus of 3 x 10(6) polymorphonuclear neutrophilic leukocytes or 1 x 10(9) platelets of human origin was applied after reperfusion, either with or without pretreating with 0.5 or 1 minimal alveolar concentration sevoflurane. The number of sequestered cells was calculated from the difference between coronary input and output. Coronary effluent was collected throughout reperfusion to measure shedding of the glycocalyx. Results Ischemia-reperfusion induced a significant increase in median (interquartile range) adhesion versus control nonischemic hearts of both leukocytes (38.9 (36.3-42.9) vs. 14.5 (13.1-16.0)%) and platelets (25.0 (22.5-27.1) vs. 9.4 (8.4-10.7)%). Shedding was evidenced by eightfold increases in washout of syndecan-1 and heparan sulfate versus basal. Sevoflurane reduced cell adhesion to near basal at 1 minimal alveolar concentration (leukocytes: 21.2% (19.2-23.9%), platelets: 11.5% (10.4-12.0%). Shedding measurements and electron microscopy demonstrated that sevoflurane-treated hearts retained much of their 200 nm-thick glycocalyx. Conclusions Sevoflurane reduces glycocalyx shedding in the postischemic coronary bed, maintaining the natural cover for endothelial adhesion molecules and, thus, reducing cell adhesion. This may explain beneficial outcomes linked to clinical use of volatile anesthetics after ischemia-reperfusion.

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