Abstract
Brief episodes of myocardial ischemia-reperfusion (IR) employed during reperfusion after a prolonged ischemic insult may attenuate the total ischemia-reperfusion injury. This phenomenon has been termed ischemic postconditioning. In the present study, we studied the possible effect of ischemic postconditioning on an ischemic reperfusion (IR)-induced myocardium oxidative injury in rat model. Results showed that ischemic postconditioning could improve arrhythmia cordis, reduce myocardium infarction and serum creatin kinase (CK), lactate dehydrogenase (LDH) and aspartate transaminase (AST) activities in IR rats. In addition, ischemic postconditioning could still decrease myocardium malondialdehyde (MDA) level, and increased myocardium Na+-K+-ATPase, Ca2+-Mg2+-ATPase, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and glutathione reductase (GR) activities. It can be concluded that ischemic postconditioning possesses strong protective effects against ischemia reperfusion-induced myocardium oxidative injury in IR rats.
Highlights
Despite the powerful protective effects of ischemic preconditioning, the clinical application of this phenomenon has been rather disappointing, mainly because preconditioning must be instituted before the ischemic event [1,2,3]
We investigate the protective effect of ischemic postconditioning on myocardium oxidative injury in IR rats
Ischemic postconditioning significantly increased the activities of myocardium superoxide dismutase (SOD), CAT, GSH-Px and glutathione reductase (GR) in experimental animals
Summary
Despite the powerful protective effects of ischemic preconditioning, the clinical application of this phenomenon has been rather disappointing, mainly because preconditioning must be instituted before the ischemic event [1,2,3]. Ischemic postconditioning (IPO) was described for the first time in Molecules 2012, 17 dogs by Zhao et al [4] These authors demonstrated that a series of repetitive cycles of brief reperfusion and reocclusion of the coronary artery applied at the onset of reperfusion after a prolonged ischemic event reduced infarct size. ROS may cause cellular damage by peroxidation of membrane lipids, sulfhydryl enzyme inactivation, protein cross-linking and DNA breakdown [26,29,30,31,32]. To counter this potential damage, organisms have enzymatic (such as superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT)) and nonenzymic (tocopherols, carotenes, ubiquinol, glutathione, ascorbic acid) antioxidant defences [27,33,34,35]. We investigate the protective effect of ischemic postconditioning on myocardium oxidative injury in IR rats
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