Myocardial contracture: the predominant causes of impeded reperfusion in simulated surgical ischemia.
"Worst-case" surgical conditions were simulated using the isolated model of a parabiotically perfused rabbit heart septum. Such conditions occur clinically in regional myocardium distal to stenosed coronary arteries and are characterized by inadequate or absent ionic influence on the myocardium by chemical cardioplegia and equilibration to room temperature. This study tested the hypothesis that ischemic contracture, rather than intracellular or extracellular edema, critical closing or delayed critical opening, was the predominant cause of impeded reperfusion that damages myocardium. In 20 reperfused ischemic septa, conductance (flow per unit pressure) decreased significantly (P less than 0.05) as ischemia at 24 degrees C was prolonged from 15 to 90 minutes and as contracture became more severe. Conductance was not decreased significantly by even large amounts of extracellular edema. Intracellular edema did not occur. In 17 normal septa, the critical closing pressure was 9.3 mm Hg. Critical opening pressures following 5 to 90 minutes ischemia at 24 degrees C did not differ significantly. Although early reflow was impeded progressively with longer ischemic intervals, it was not significant as was due to contracture rather than critical closing or delayed critical opening. This study confirmed the hypothesis that contracture is the predominant cause of impeded reperfusion in simulated surgical ischemia.
D000818:Animals; D003286:Contracture / Q000503:physiopathology*; D003326:Coronary Circulation; D006321:Heart / Q000503:physiopathology*; D006324:Heart Arrest, Induced; D008297:Male; D008954:Models, Biological; D009200:Myocardial Contraction; D011817:Rabbits