The relationship between myocardial contracture and cell calcium was studied in electrically paced, isolated perfused rabbit hearts. Isovolumic left ventricular dP/dt and end-diastolic pressure were utilized as indexes of contractility and ventricular stiffness. After 60 min of low flow (ischemia) without or with reperfusion at high flow for 10 min, calcium was measured in the mitochondrial fraction and used as an indicator of intracellular calcium. Low flow led to ventricular standstill and contracture, and reperfusion produced partial mechanical recovery with end-diastolic pressure remaining markedly elevated. Nifedipine (10(-7) M), an antagonist of myocardial calcium uptake, prevented contracture and permitted nearly complete mechanical recovery without elevation in diastolic pressure. Increases in mitochondrial calcium paralleled the severity of contracture and the lack of diastolic relaxation after reperfusion. Mitochondrial calcium did not increase in hearts protected by nifedipine. Results demonstrate a close relationship between mechanical changes induced by ischemia and accumulation of intracellular calcium.