CORONARY FLOW RESERVE AFTER ISCHEMIA AND REPERFUSION OF THE ISOLATED HEART - DIVERGENT RESULTS WITH CRYSTALLOID VERSUS BLOOD PERFUSION

Mechanical function and coronary hemodynamics were assessed in 73 isol ated rabbit hearts randomly subjected to 0, 10, 20, 30, or 45 minutes of 37 degrees C global ischemia and 45 minutes of reperfusion in eithe r a modified Krebs buffer or homologous blood-perfused Langendorff mod e (n = 7 to 9 hearts per group). Isovolumic developed pressure, restin g coronary flow, and response to endothelium-dependent (bradykinin) an d -independent (nitroglycerin) agonists were quantitated at defined pr eload and heart rate. Perfusate did not influence systolic performance , which was impaired after 30 minutes of ischemia and fell to 64% to 7 2% of preischemic values after 45 minutes of ischemia (p < 0.05). Howe ver, basal coronary how was at least sixfold greater in crystalloid-pe rfused hearts. Moreover, coronary hyperemia (p < 0.05) persisted for K rebs-perfused hearts subjected to all but the longest ischemic interva l. After equilibration, all postischemic blood-perfused hearts had bas al flow unchanged from before ischemia. Bradykinin and nitroglycerin i nduced similar increases in coronary flow for each group before and af ter each ischemia interval. However, the magnitude of this increase wa s greater in blood-perfused hearts (p < 0.01) and was not attenuated b y the ischemic times encompassed in this protocol. In contrast, endoth elium-dependent and -independent coronary flow reserve was abolished a fter 20 minutes of ischemia or longer in Krebs-perfused hearts. These data suggest that the unphysiologic resting how patterns of crystalloi d-perfused isolated hearts obfuscate interpretation of the interaction between coronary flow reserve and ischemic injury.