Essential contribution of thrombocytes to the occurrence of catecholamine-induced cardiac necroses.

The role of thrombocytes in the production of isoproterenol-induced cardiac necrosis was investigated in rats rendered thrombocytopenic (A) as well as in rats treated with a prostacyclin analogue (B). According to quantitative morphometric evaluation the area of necrotic tissue amounted to about 1% 9 h following administration of isoproterenol (40 mg/kg). In both groups of treated animals the number and area of necroses were strongly reduced (to 23% group A, to 34% group B, P less than or equal to 0.1 for both groups). In contrast, the reduction of myocardial adenine nucleotide levels induced by isoproterenol was the same (5.06 to 3.57 and 3.60 microM/g wet wt, respectively) in thrombocytopenic and non-thrombocytopenic rats. Quantitative comparison of the fraction of necrotic tissue and of the fraction of lost nucleotides suggests that non-necrotic rather than necrotic tissue predominantly contributes to the reduction of nucleotides. The dependence of cardiac necrosis production on the presence or normal aggregability of platelets points out at platelet-dependent microvascular alterations as a main cause of isoproterenol-induced cardiac necroses.