BACKGROUND: It has been found that sterss challenge with heat shock produces the acquisition of cellular resistance to ischemin injury in the hearts, which is associated with stress protein induction. The conventional heat shock(42degrees C of rectal temperature for 15min, anesthetized animal), however, is strong enough to endanger the animal life and then not suitable for practiocal application in human. The present study was performedd in an attempt to search the safely applicabel stress modalities to acquire the myocardial tolerance to ischemia-reperfusion in jury. METHODS: Male, Sprague-Ddawley rats(200-250g) were exposed to various stressful conditions, such as heat stimulation(environmental temperature of 42degrees C for 30min, live animal), swimming(20min), immobilization(60min), treadmill exercise(20M/min, 30min) and hyperbaric oxygenation(3atm, 60min) given once a day for 5 days. Twenty-four hours after the last application the hearts were isolated and perfused with oxygenated Krebs-Henseleit buffer solution by Langendorff method. Ischemia-reperfusion injury was produced by 20 min-global ischemia followed by 30 min-reperfusion. Cardiac mechanical function, lactate dehydrogenase release, the induction of stree proteins were assayed and compared dbetween the stressed dand the control animals. RESULTS: Upon reperfusion after ischemia the recovery of cardiac function was significantly improved in the stressed animals. The percentile recovery at 30min of reperfusion was in a range from 55.3%(swimming) to 89.3%(treadmill exercise), which was significantly higher than that of the control hearts(38%). The functional recovery of the conventional heat shocked heart was 57.7%. In stressed animals, lactate dehydrogenase release, which indicates myocardial cell injury, was significantly reduced by 20 to 30% compared to that for the control. The expression of an inducible form of 70 series stress protein, SP72, which was assayed by immunoblotting method, was markedly increased by heat stimulation while the other stress modalities failed to increase, it. There were no appreciable inductions of SP73(constitutive form) and GRR78 in the stressed animals. CONCLUSION: These results suggest that the cardiac protection from the ischemia-reperfusion injury could be induced by the repetitive non-fatal stress stimulations and that SP70 family proteins may be partly involved in the cardioprotective effect produced by heat stimulation, but not play the essential roles in anti-ischemic effects produced by other stress modalities.