Transient Drug-Induced Myocardial Dysfunction is Not Ameliorated by PGI2 in Dogs

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Abstract
Prostacyclin (PGI2), a potent vasodilatory substance that effectively inhibits platelet aggregation was under clinical investigation for the treatment of angina pectoris. The effects of PGI2 on transient drug-induced myocardial dysfunction were studied in anesthetized, thoracotomized dogs. Regional myocardial function was assessed using 2 pairs of piezoelectric transducers and a multidimensional measuring gauge; 1 pair was implanted in the distribution area of the left circumflex branch (LCX) and the other in the distribution area of the descending branch (LAD) of the left coronary artery. After i.v. injection of isoproterenol (ISO), which led to an increase in systolic shortening in the LCX and LAD areas, a critical stenosis was performed on the LCX and maintained at this level. I.v. ISO injection now induced regional dysfunction in the LCX-dependent segment with the occurrence of systolic bulging. Infusion of PGI2 at a dosage of 100 ng/kg per min caused a decrease in arterial blood pressure and an increase in heart rate, but had no effect on regional myocardial function. ISO-induced myocardial dysfunction in the critically stenosed LCX segment, which was observed before PGI2 administration, was not ameliorated, but rather aggravated, by PGI2. PGI2 does not improve normal or ISO-stimulated myocardial function in pressure-dependent perfused areas of the heart.