The effect of K+ (13.5 and 26 mmol). Cs+ (10 mmol), verapamil (500 nmol) and desipramine (100 nmol) added to the perfusate before the induction of 25-min total ischemia on the release of noradrenaline (NA) and adenine nucleotide degradation products (ANDP) and on myocardial contractility recovery has been studied on the isolated guinea-pig heart. It has been shown that desipramine-induced inhibition of catecholamine transport through axoplasmic membrane was accompanied by a considerable decrease in NA and ANDP release from ischemic myocardium. The experiments on KCl, CsCl and verapamil have demonstrated that the degree of preischemic contractility reduction determines ANDP myocardial loss and contractility recovery in reperfusion. Linear correlation observed in all the experimental series between the degree of endogenous NA release and overall ANDP release suggests that the magnitude of NA release in ischemia is determined by the energetic myocardial status. NA loss approaches zero if adenine nucleotide pool is not reduced to minimal critical values.