Do neutrophils mediate the phenomenon of stunned myocardium?

Abstract

Brief periods of transient ischemia have been associated with prolonged postischemic dysfunction-the syndrome of stunned myocardium (1). In the canine model of 15 min of coronary artery occlusion followed by reperfusion, recovery of function may require hours to days despite the absence of tissue necrosis (2,3). Biochemical abnormalities have been observed in stunned myocardium: subendocardial adenosine triphosphate (ATP) levels are reduced for at least 3 days after reperfusion of a coronary artery subjected to IS min of occlusion (4). Stunned myocardium has been observed in patients receiving thrombolytic therapy for acute evolving myocardial infarction, as well as in patients undergoing exercise stress testing (5). Mechanisms of myocardial stunning. There have been several proposed mechanisms for the phenomenon of stunned myocardium, including altered calcium flux, oxygen free radical damage and abnormal energy utilization (6). Oxygen free radicals have been implicated as a cause of stunned myocardium by a number of investigators (7-9). These cytotoxic species such as superoxide anion and hydroxyl radical are known to be generated during ischemia and reperfusion (10). Oxygen free radicals recently have been documented in the coronary vein effluent of a canine model of 15 min of ischemia and reperfusion by utilizing electron paramagnetic resonance spectroscopy and a spintrapping agent (10). In addition, oxygen radicals have been shown to inhibit the function of isolated sarcolemmal membrane preparations (11) and to depress function of isolated papillary muscle preparations (12). Several independent laboratories (7-9,lO) including our own (8) have observed that administration of oxygen free radical scavengers, such as superoxide dismutase plus catalase, enhances the return of function of myocardium subjected to 15 min of ischemia