CORONARY BLOOD-FLOW AUTOREGULATION AND FLOW HETEROGENEITY IN THE STUNNED HEART

We used an anesthetized swine model of regionally ''stunned'' myocardi um to determine the effect of stunning on coronary autoregulation and blood flow heterogeneity. In 18 domestic swine, stunning was accomplis hed by reducing blood flow to the left anterior descending coronary ar tery (LAD) by approximately 75% of baseline for 15 min and restoring i t to normal for 1 hour. We quantified coronary autoregulation using bo th the slope of coronary pressure-flow curves and an autoregulation in dex. We quantified blood flow heterogeneity using radioactive microsph eres to determine the variability in flow (dispersion index) among for ty 200 mg segments of myocardium from the center of the stunned, LAD-p erfused left ventricle. Before and after stunning, we measured autoreg ulation, myocardial blood flow and flow heterogeneity, as well as hemo dynamic indices of myocardial oxygen demand. Fifteen min of ischemia a nd 1 hour of reperfusion produced both a 46% reduction in mechanical f unction, and a 7% drop in systemic arterial pressure, but no change in heart rate or rate pressure product. Myocardial oxygen consumption wa s 15% reduced and myocardial blood flow 16% reduced in the stunned myo cardium when measured at one hour of reperfusion. Fifteen min after re perfusion, the slope of the coronary pressure flow plots and the coron ary venous oxygenation were increased whereas the autoregulation index decreased. These findings all indicate reduced autoregulation during early reperfusion. However, after one hour of reperfusion, the slope o f the coronary pressure-flow relation (0.41 +/- 0.19 vs. 0.48 +/- 0.26 ml.100 g-1.min-1.mmHg-1) and the autoregulation index (0.43 +/- 0.16 vs. 0.30 +/- 0.32) were unchanged from control measurements (p > 0.05) . Blood flow heterogeneity remained normal in the stunned myocardium. These findings challenge the hypothesis that the mechanical dysfunctio n of the stunned myocardium is due to suboptimal perfusion resulting f rom poor coronary autoregulation or maldistribution of blood flow.