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Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium.
The multiple anginal episodes that often precede myocardial infarction in man may delay cell death after coronary occlusion, and thereby allow for greater salvage of myocardium through reperfusion therapy, which is proposed to protect the heart from a subsequent sustained ischemic insult. Expand
The "no-reflow" phenomenon after temporary coronary occlusion in the dog.
Results suggest that 40 minutes of ischemia were tolerated by the capillary bed of the dog heart without serious capillary damage or perfusion defects, but that 90 min of ischemic injury was associated with the "no-reflow" phenomenon, i.e., failure to achieve uniform reperfusion. Expand
The "wavefront phenomenon" of myocardial ischemic cell death. II. Transmural progression of necrosis within the framework of ischemic bed size (myocardium at risk) and collateral flow.
Eventual transmural necrosis, and therefore over-all infarct size was determined by, and can be predicted from flow measurements obtained shortly after coronary occlusion, and irreversible injury of ischemic myocardium developed as a transmural wavefront. Expand
The Wavefront Phenomenon of Ischemic Cell Death: 1. Myocardial Infarct Size vs Duration of Coronary Occlusion in Dogs
The results document the presence of a subepicardial zone of ischemic but viable myocardium which is available for pharmacologic or surgical salvage for at least three and perhaps six hours following circumflex occlusion in the dog. Expand
Ischemic preconditioning slows energy metabolism and delays ultrastructural damage during a sustained ischemic episode.
It is proposed that preconditioning reduces myocardial energy demand during ischemia, which results in a reduced rate of high energy phosphate utilization and a reducedRate of anaerobic glycolysis, which is responsible for delaying ischemic cell death. Expand
The cell biology of acute myocardial ischemia.
The metabolic changes associated with the sudden onset of ischemia caused by occlusion of a major coronary artery include (a) cessation of aerobic metabolism, (b) depletion of creatine phosphateExpand
Consequences of brief ischemia: stunning, preconditioning, and their clinical implications: part 1.
That preconditioning may occur in humans is suggested by the observations that repetitive balloon inflations in the coronary artery are associated with progressively less chest pain, ST-segment elevation, lactate production, the protective effects of preinfarction angina, the anginal "warm-up phenomenon," and studies performed on human cardiac biopsies that show metabolic properties suggesting preconditionsing. Expand
Myocardial calcium and magnesium in acute ischemic injury.
Investigation of the localization of the increased Ca(--) by cellular fractionation and chemical analysis as well as by electron miscroscopy and microincineration showed that much of it was localized in dense bodies within the mitochondria. Expand
Structural Changes in Myocardium During Acute Ischemia
Findings suggest that failure of cell volume regulation may be one of the earliest signs of the development of the irreversible phase of ischemic injury. Expand