Mechanisms of myocardial ischemic injury assessed by phosphorus-31 magnetic resonance spectroscopy (effects of catecholamine on ischemic hearts).

To investigate the mechanisms of development in ischemic myocardial injury, intracellular pH and high energy phosphates in perfused guinea-pig hearts were measured using 31P-MRS method. During 60 minutes' global ischemia, intracellular ATP level decreased to 1.2% and 26.4% of control, respectively with and without preischemic administration of isoproterenol, while intracellular pH declined to 6.48 and 6.03. In hearts loaded with isoproterenol, approximately 50% of ATP was depleted with little pH decline. After 40 minutes' reperfusion with a standard perfusate, ATP levels were 23.3% and 46.1%. Cardiac contractility (LVdp/dt) were 16.3% and 45.0% of control value respectively. When hearts were reperfused with inosine, cardiac functions recovered to 52.3% and 81.6% respectively with and without preischemic administration of isoproterenol, while ATP increased to 59.4% and 78.1% after 6 hours' reperfusion. Recovery of ATP level correlated with recovery of contractility. Isoproterenol stole the ability of ATP synthesis from a plenty of ischemic myocytes and progressed irreversible myocardial ischemic injury. ATP depletion was a critical factor in the onset of irreversibility rather than accumulation of anerobic glycolytic products. Measurement of ability of ATP synthesis, with administration of inosine, was supposed to be an usable method to evaluate any organ's viability using 31P-MRS.