The role of intracellular calcium in the ischemic myocardial damage

The isolated, perfused ventricles of guinea-pig and rat hearts stimulated at the rate of 60/min were equilibrated for 60 min with 45Ca containing solution. Thereafter some of them were perfused for the last 10 min of experiment with deoxygenated (pO2 = 35 not equal to 7 mm Hg) radioactive solution. Hypoxia resulted in decrease of exchangeable calcium (45Ca) content by 0.90 mmol/kg w.w. in guinea-pig and by 0.26 mmol/kg w.w. in the rat. The amount of 15Ca lost by guinea-pig ventricles is equal to the content of rate-dependent fraction Ca2 described in the previous papers [Pytkowski et al., 1983; Lewartowski et al., 1984]. The isolated papillary muscles of the right ventricles of guinea-pig and rat hearts were subjected to 90 min of ischemia simulated by immersion in the warm, deoxygenated paraffin oil. Some of the guinea-pig muscles were deprived of Ca2 fraction by means of prolonged rest (20 min) immediately prior to ischemia. All the preparations were quiescent during ischemia. The guinea-pig muscles deprived of fraction Ca2 and the rat muscles developed much weaker contracture during ischemia and showed better recovery of phasic contraction upon reperfusion than the guinea-pig muscles containing Ca2 fraction prior to ischemia. We propose that Ca2 fraction is released from its binding sites at the early phases of ischemia contributing to the disturbances in Ca homeostasis and to mechanism of damage of ischemic cardiac muscle.