Reperfusion of ischemic myocardium is crucial for salvaging myocardial cells from ischemic cell death. However, reperfusion itself induces various deleterious effects on the ischemic myocardium. These effects, known collectively as reperfusion injury, comprise stunned myocardium, reperfusion-induced arrhythmia, microvascular reperfusion injury, and lethal reperfusion injury. No approach has pro...

conclusions pretreatment with epo and application of ipc significantly ameliorated the renal injury induced by bilateral renal ir. however, both treatments attenuated renal dysfunction and oxidative stress in kidney tissues. there were no significant differences between pretreatment with epo or application of ipc. materials and methods twenty four male wistar rats were allocated into four exper...

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. Resu...

BACKGROUND It is well known that propofol protects myocardium against myocardial ischemia/reperfusion injury in the rat heart model. The aim of this study was to investigate whether propofol provides a protective effect against a regional myocardial ischemia/reperfusion injury in an in vivo rat heart model after 48 h of reperfusion. METHODS Rats were subjected to 25 min of left coronary arter...

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 mechan...

Background—Ischemic heart disease is the greatest cause of death in Western countries. The deleterious effects of cardiac ischemia are ameliorated by ischemic preconditioning (IPC), in which transient ischemia protects against subsequent severe ischemia/reperfusion injury. IPC activates multiple signaling pathways, including the reperfusion injury salvage kinase pathway (mainly PI3K-Akt-glycoge...

Acute myocardial infarction (AMI) is the leading cause of death, morbidity, and health costs worldwide. In AMI, a sudden blockage blood flow causes ischemia cell death. Reperfusion after has paradoxical effects may exacerbate injury, process known as ischemic reperfusion injury. this work we evaluated lipidome isolated rat hearts, maintained in controlled perfusion (CT), undergoing global (ISC)...

conclusions the results suggest the important role of the antioxidant system potentiation in the prevention of myocardial damage. results cell degenerative changes, pyknotic nuclei, contraction bands, edema, and loosening of collagen in between muscle fibers were observed during ischemia-reperfusion. myocardial architecture and cellular morphology were recovered in co-administration groups, esp...

Several lines of evidence suggest that proteasomes are involved in multiple aspects of myocardial physiology and pathology, including myocardial ischemia-reperfusion injury. It is well established that the 26S proteasome is an ATP-dependent enzyme and that ischemic heart disease is associated with changes in the ATP content of the cardiomyocyte. A functional link between the 26S proteasome, myo...

OBJECTIVE Matrix metalloproteinase-9 (MMP-9) activity is up regulated in the heart subjected to ischemic insult. Whether increased MMP-9 activity contributes to acute myocardial injury after ischemia-reperfusion remains unknown. To investigate the role of MMP-9 in myocardial infarction, we utilized a MMP-9 knockout mouse. METHODS AND RESULTS Standard homologous recombination in embryonic stem...