Recovery of heart contractility after global normothermic ischemia in New-Zealand rabbits depends on the reperfusion mode and the composition of reperfusion medium and correlates with mitochondrial respiration. Cardiac function can recover also at low ATP concentration (about 1 gmol/g dry tissue). Key Words: rabbit heart; ischemia; reperfusion; mitochondrial respiration; high-energy phosphatesDeep myocardial ischemia reduces tissue content of high-energy phosphates, in particular ATP and creafine phosphate (CP), due to inhibition of oxidative phosphorylation in mitochondria followed by lactate accumulation and enhanced glycogen decomposition. It has been shown that ATP plays an essential role in the development of ischemia-induced myocardial damage [2,4,11]. These studies also demonstrated that myocardial contractility can be restored if the ischemized tissue contains at least 2-3 gmol ATP per gram dry tissue, whereas lower ATP content leads to irreversible changes in cardiomyocytes and loss of contractility [3,7,8]. We assume that under conditions of preserved mitochondrial functions the contractility of myofibrils can be restored even at negligible or zero tissue ATP content. Since tissue ATP content corresponds to the difference between ATP synthesis and degradation, the absence of ATP accumulation during reperfusion may imply its complete utilization. It should be noted that these studies were carried out on the model of regional hypothermic ischelnia with cardioprotection. Mitochondrial respiration was assessed on isolated mitochondria. It is known that considerable proportion of the mitochondria is lost during isolation, particularly from Azerbaijan Medical University, Balm damaged tissues, which masks the real picture and the degree of damage [t0].We investigated the relationship between mechanical function of the myocardium and the rate of mitochondrial respiration and ATP content during reperfusion after normothermic global ischemia. MATERIALS AND METHODSHearts isolated from New Zealand rabbits weighing 1.7-2.0 kg were perfused via the aorta with KrebsHenseleit buffer (Langendorff retrograde perfusion at constant pressure without recirculation) [1]. Before ischemia and during reperfusion the hearts were arrested with St. Thomas's Hospital cardioplegic solution, pH was measured "after carbogen saturation (95% 02, 5% CO2) at 37~ 10 mM CP (disodium salt) and 15 mM glutamaic acid (GA, potassium salt) were added to the cardioplegic solution as cardioprotectors (CP-containing solution with 90 mM NaC1). To model global ischemia the perfusate flow was interrupted; hypothermia (22~ and cardioprotectors were used only during reperfusion with cardioplegic solution.The hearts were perfused before ischemia (group 1), subjected to 80-rain cardioplegic normothernfic ischemia (group 2), and reperfused under different