Hypothermia in a heart in which coronary circulation is sustained produces positive inotropism of the myocardium. The effects on cardiac function and intracellular Ca profile of rapid cooling shock (RCS) immediately after reperfusion were evaluated in terms of their ability to inhibit the onset of myocardial stunning and to rapidly improve function. RCS administered to isolated hearts of Langendorff perfusion rats for 3 minutes induced positive inotropism after 32 +/- 4 seconds, with LV Developed Pressure (LVDP) increased a normal 120 +/- 10% (mean +/- SE, n = 16). Based on the result in which the positive inotropism was confirmed, an experiment using rats was performed as follows: after 30 minutes of ischemia at 37 degrees C, 25 degrees C or 10 degrees C, the hearts were reperfused for 1, 2 or 3 minutes and RCS was administered for 1, 2 or 3 minutes. LVDP was satisfactorily reversed early in rats treated with RCS for 3 minutes after 3 minutes reperfusion of the ischemic hearts at 25 degrees C. In this group, no significant change in Ca concentration in myocardial cells was observed at reperfusion: +/- 3% of the baseline level. Intracellular Ca overload at reperfusion and decreased intracellular Ca level, which have the effect of suppressing the CICR channel, which plays a role in Ca release into the sarcoplasmic reticulum at contraction, are important causative factors in the development of myocardial stunning, as are free radicals. RCS improved myocardial function rapidly because it inhibited change in Ca level.