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.
D000818:Animals; D001792:Blood Platelets / Q000187:drug effects / Q000502:physiology*; D009202:Cardiomyopathies / Q000209:etiology* / Q000473:pathology; D002395:Catecholamines / Q000494:pharmacology*; D005260:Female; D007545:Isoproterenol / Q000633:toxicity; D008833:Microcirculation / Q000187:drug effects; D009336:Necrosis; D010974:Platelet Aggregation; D051381:Rats; D011919:Rats, Inbred Strains; D013921:Thrombocytopenia / Q000503:physiopathology
D002395:Catecholamines; D007545:Isoproterenol