Myocardial ischemia/reperfusion injury affects not only the cardiomyocyte compartment but also all other cellular compartments, and the coronary circulation has a central role in it. Acute myocardial infarction most often arises from atherosclerotic plaque rupture/erosion with superimposed thrombosis (type 1 myocardial infarction). However, in the absence of coronary atherosclerosis, coronary v...

We have previously demonstrated that simvastatin attenuates myocardial cell necrosis after acute myocardial ischemia and reperfusion via induction of endothelial cell NO synthase. However, it remains unknown whether the cardioprotective effects of statins can persist after extended periods of reperfusion. Furthermore, it is unknown whether simvastatin therapy can attenuate postischemic cardiac ...

Successful treatment of myocardial infarction related to early reperfusion therapy has caused growing interest in not only ischemic but also myocardial reperfusion injury. Most experimentally confirmed preservation myocardial reperfusion injury methods have failed in clinical practice. Probably one reason for their ineffectiveness was the very narrow "time window" necessitating application of p...

Coronary artery thrombosis, due either fissuring or erosion of atherosclerotic plaque, is the usual cause of acute myocardial infarction (1) and results in a progressive increase of the infarct size with a wavefront transmural extension from the endocardium towards the epicardium (2,3). Although thrombolysis and reperfusion can occur spontaneously, thrombotic coronary artery occlusion usually p...

Serial myocardial imaging with technetium-99m methoxyisobutyl isonitrile (99mTc-MIBI) has been proposed for evaluating myocardial salvage after reperfusion. To define 99mTc-MIBI uptake before and after reperfusion, 17 open-chest dogs underwent 3 hours of left anterior descending artery occlusion and 3 hours of reperfusion. 99mTc-MIBI was injected during occlusion (group 1) or after 90 minutes o...

Myocardial sulfhydryl (SH)-containing compounds, including reduced glutathione (GSH), are both defenses against and potential markers of reactive oxygen metabolite injury during ischemia and reperfusion. We examined the alterations in GSH and other myocardial SH pools during reperfusion in anesthetized dogs exposed to brief (15 minutes, n = 7) or prolonged (90 minutes, n = 6) regional ischemia ...

BACKGROUND Reperfusion injury of ischemic myocardium has been attributed to neutrophil infiltration, inflammatory activation and cardiac necrosis/apoptosis. Serine protease inhibition with aprotinin is cardioprotective, but the mechanism is unknown. METHODS AND RESULTS We studied aprotinin in a rat model of myocardial ischemia for 20 minutes and reperfusion for 20 minutes, 8 hours or 24 hours...

Serial myocardial imaging with technetium-99m methoxyisobutyl isonitrile (9'Tc-MIBI) has been proposed for evaluating myocardial salvage after reperfusion. To define 'mTc-MIBI uptake before and after reperfusion, 17 open-chest dogs underwent 3 hours of left anterior descending artery occlusion and 3 hours of reperfusion. 9'Tc-MIBI was injected during occlusion (group 1) or after 90 minutes of r...