Myocardial reperfusion injury. Histopathological effects of perfluorochemical.

Abstract

Regional myocardial ischemic injury progresses as a "wave-front" phenomenon from the endocardium to the epicardium. Myocyte damage can be reversible or irreversible and is dependent on the duration of ischemia. Endothelial cell injury lags behind myocyte injury. Reperfusion of ischemic myocardium can result in the acceleration of endothelial injury with resultant conversion of surrounding reversibly injured myocytes to irreversible damage; this has been termed the "no-reflow" phenomenon. This process can be accelerated by the presence of neutrophils. Agents such as perfluorochemicals and adenosine, which attenuate endothelial injury and inhibit neutrophil infiltration, also reduce infarct size in animal models. Infarct size reduction with perfluorochemical was observed with both intracoronary and intravenous infusion. Infarct healing was not adversely affected except for the persistence of perfluorochemical-laden macrophages. These studies suggest that perfluorochemicals and adenosine might be beneficial adjuvants to thrombolytic therapy in the reduction of reperfusion injury.