Background: Calcium overload and free radical mediated damage in the mitochondria is the most important pathological changes associated with myocardial ischemic-reperfusion injury. The verapamil post-treatment has been previously reported to prevent reperfusion-induced myocardial injury but functional recovery may be delayed due to the drug's inherent direct myocardial depression effect. In the...

background: calcium overload and free radical mediated damage in the mitochondria is the most important pathological changes associated with myocardial ischemic-reperfusion injury. the verapamil post-treatment has been previously reported to prevent reperfusion-induced myocardial injury but functional recovery may be delayed due to the drug's inherent direct myocardial depression effect. in the...

Introduction: Reactive oxygen species (ROS) have been suggested to play an important role in the myocardial damage induced by ischemia – reperfusion. One element believed to be activated by ROS and to contribute to the reduction of ROS production, is the uncoupling protein-2 (UCP2). The objective of this investigation was to explore the effect of myocardial ischemia reperfusion on cardiac UC...

introduction: nicotinamide adenine dinucleotide phosphate (nadph) oxidase-2 (nox2) is one of the predominant sources of ros production during myocardial ischemia-reperfusion and can be induced by angiotensin ii. the evidence suggests that pharmacological blockers of renin-angiotensin system can exert direct tissue effects independent of their ability to regulate blood pressure. the mechanism(s)...

Introduction: Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-2 (Nox2) is one of the predominant sources of ROS production during myocardial ischemia-reperfusion and can be induced by angiotensin II. The evidence suggests that pharmacological blockers of renin-angiotensin system can exert direct tissue effects independent of their ability to regulate blood pressure. The mechanism...

the anti-apoptotic gene bcl-2 is located in mitochondria, but it is uncertain whether its expression affects hepatocyte survival in ischemia/reperfusion (i/r) injury. this experiment was designed to evaluate the role of folic acid in expression of bcl-2 in i/r in rat liver. eighteen wister rats were divided into sham-operated controlgroup (c) (n=6), i/r group (n=6), folic acid treated group whi...

organ damage after reperfusion of previously viable ischemic tissues is defined as ischemia/reperfusion injury. the pathophysiology of ischemia/reperfusion injury involves cellular effect of ischemia, reactive oxygen species and inflammatory cascade. protection against ischemia/reperfusion injury may be achieved by preconditioning or postconditioning. in this review, we discuss basic mechanisms...

objective(s)ischemia-reperfusion injury (iri) is a leading cause of kidney transplantation failure, and ischemic-preconditioning (ipc) is a protective method against the iri. in the present study, the defensive effect of ipc on rats’ kidney was investigated and more importantly the differences between two genders were appraised.materials and methodsthirty two wistar rats were randomly allocated...

background: the role of nitric oxide (no) of endothelial or neuronal origins in cerebral ischemia and reperfusion injuries are far from being settled, extending from being important to not having any role at all.    objective: to investigate the role of no of endothelial and neuronal origins in ischemia/reperfusion injuries in focal cerebral ischemia, l-name, a non selective no synthase inhibit...

background: the role of renin angiotensin system (ras) in ischemic/reperfusion (i/r) injuries is not fully elucidated. furthermore, it is not clear whether inhibition of ras by angiotensin-converting enzyme (ace) inhibitors has beneficial effects in terms of protecting the brain from i/r injuries. in this study enalapril is used as an ace inhibitor to evaluate the role of ras in i/r injuries in...