Relative roles of edema versus contracture in the myocardial postischemic “no-reflow” phenomenon

Abstract

Failure to reestablish blood flow to the subendocardium of the left ventricle may occur after prolonged myocardial ischemia and it has been suggested that edema may be responsible for this “noreflow” phenomenon. However, the process of ischemic contracture is also associated with prolonged myocardial ischemia and an inability to reperfuse the subendocardium. This study was designed to clarify the relative roles of edema and contracture in the pathogenesis of subendocardial “no-reflow.” This objective was achieved by determining the transmural distribution of tissue blood flow and water content across the wall of the left ventricle, in both the presence and absence of contracture, during the reperfusion phase after global myocardial ischemia of sufficient duration to exhaust myocardial anerobic metabolism. We made use of the fact that ischemic contracture can be inhibited in the intact canine heart by decreasing the temperature to a level of moderate hypothermia (28°C) in order to separate the variables of contracture and edema. We found that the subendocardial “no-reflow” phenomenon was present when contracture was present, but absent when contracture was absent. While edema, assessed by tissue water contents in excess of control values, was much greater in the deeper layers of the left ventricular wall in the absence of contracture than in its presence, there was no evidence that it impeded myocardial blood flow. Edema was indeed found to be greater in regions of greater flow. These findings challenge the concept that myocardial edema following ischemic arrest in cardiac surgery is directly responsible for inadequate reperfusion leading to necrosis.