Role of prostacyclin in the preservation of ischemic myocardial tissue in the perfused cat heart.

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Abstract
Prostacyclin (PGI2) and some of its major breakdown products (6-keto-PGF1a, 6-keto-PGE1 and 13,14-dihydro 6,15-diketo-PGF1a) were studied in an isolated perfused cat heart preparation during myocardial ischemia. At an infusion rate of 10 ng/g heart weight per minute.PGI2 and the related compounds caused no changes in perfusion pressure, contractile force (CF) the 1st derivative of the contractile force (dF/dt) and heart rate in control hearts perfused at coronary flows of 20-35 ml/min. Induction of global ischemia by perfusion at 0.6-0.7 ml/min for 120 min caused a significant release of creatine kinase (CK) activity and compounds having a free amino-N group into the perfusate. Ischemic hearts exhibited an increase in resting tension of 2.3 .+-. 0.2 g, mean .+-. SEM [SE of mean]. Upon reperfusion, untreated ischemic hearts showed a partial restoration of mechanical performance, CF = 43 .+-. 5%, and dF/dt = 40 .+-. 5% of control. PGI2 infusion inhibited the ischemic-induced CK release and the increase in perfusate amino-N concentration. Resting tension remained low (i.e., 0.8 .+-. 0.1 g). Recovery of CF and dF/dt upon reperfusion was significantly higher (86 .+-. 8% and 88 .+-. 10%, respectively) than in the untreated ischemia group. Myocardial CK activity was significantly higher in PGI2-infused hearts (35.8 .+-. 2.6 IU/mg protein) compared to those infused with its vehicle (26.3 .+-. 2.8, P < 0.01). Breakdown products of PGI2 only slightly protected against ischemia. PGI2 is beneficial in myocardial ischemia in vitro, even without its wellknown action preventing platelet aggregation and independent of its induction of coronary vasodilation.