Reperfusion effect upon ischemic myocardial injury

Abstract Coronary artery ligation with or without reperfusion was carried out in Wistar rats to study the role of reperfusion upon ischemic cardiac muscle cell injury by using the fine structural extracellular protein tracer, horseradish peroxidase (HRP). The findings were compared with those obtained following administration of norepinephrine, a pressor and isoproterenol, a depressor catecholamine. Following the ligation of the left coronary artery that lasted for 20 min some of the collaterals in the ischemic zone were perfused by the tracer, but the number of patent capillaries decreased during a 60-min ligation. The non-homogeneous involvement of cardiac muscle cells in ischemic injury correlated well with these microcirculatory findings. Following a 60-min sustained occlusion, HRP reaction product was visualized on ribosomes and on external mitochondrial membranes of altered cardiac muscle cells. As contrasted with the findings following an identical period of permanent ischemia, after reperfusion an abrupt deterioration of the cardiac muscle cell alteration occurred with influx of plasmatic substances into altered cardiac muscle cells; also the localization of tracer was strikingly different as HRP was bound to contracted myofilaments. The similarity of the changes in the cardiac muscle cell to that seen in the catecholamine models, suggests that in addition to microcirculatory factors, direct cardiac muscle cell stimulation, possibly through release of catecholamines, may also play a role in the evolution of reperfusion injury.