The effects of metabolic acidosis and alkalosis in the initial reperfusate on post-ischemic stunned myocardium were investigated in isolated rat hearts. Metabolic acidosis and alkalosis were produced by altering the doses of artificial buffer (Tris) in place of sodium bicarbonate. All hearts were subjected to global ischemia for 15 min at 37 degrees C. The initial reperfusate under study was given during the subsequent 10 min of reperfusion, just prior to release of the aortic clamp. After that, reperfusion using normal Krebs-Henseleit buffer solution was carried out for 40 min. The acidotic initial reperfusate (pH 6.8) resulted in better protection than the alkalotic initial reperfusate (pH 7.8), as demonstrated by 1) a higher recovery of aortic flow (80.6% +/- 3.8% vs 32.7% +/- 4.8%, p less than 0.01), 2) a smaller leakage of creatine kinase during the initial reperfusion phase (6.0 +/- 0.7 vs 14.6 +/- 2.1 IU/10 min/g dry weight, p less than 0.05) and during the post-ischemic Langendorff perfusion phase (8.8 +/- 1.7 vs 37.3 +/- 5.2 IU/10 min/g dry weight, p less than 0.05), and 3) a lower myocardial water content at the end of reperfusion (84.8% +/- 0.2% vs 85.7% +/- 0.3%, p less than 0.05). Not only Tris buffer system, but also HEPES buffer system indicated that acidotic initial reperfusate was effective to protect against myocardial injury. These results suggest that 1) the extracellular pH during initial reperfusion profoundly influences the reversible myocardial dysfunction (stunned myocardium), and 2) the acidotic initial reperfusate improves post-ischemic myocardial performance.