[Thrombocytopenic diathesis after gentamicin--case report].

A case is described of gentamicin induced thrombocytopenic diathesis in 65-year old woman. Pathogenesis of drug induced thrombocytopenia is briefly discussed as well as outlines of treatment.

[Morphologic reflection of protein biosynthesis disorders in the myocardial cells of rabbits with acute diphtheritic intoxication].

The lethal dose of diphtheria toxin (IDLM per 1 kg of body weight) was injected to Chinchilla line adult rabbits. Histological and electron-microscopy investigations were carried out in time periods from 3 to 24 hours following the administration of the toxin. Degenerative and necrotic changes in the myocardial cells under conditions of the given experiment were not observed.

[The effect of acetylsalicylic acid on the development of infarct-like myocardial necroses experimentally induced in rats by a single administration of novodrin (isopropylnoreadrenaline)].

It appeared that acetylsalicylic acid considerably decreased both development of the infarction-like foci of necrosis and primary damage of the myocardial cells experimentally induced in animals by direct action of novodrin and expressed in the course of the first hour. This led to the supposition that acetylsalicylic acid not only prevented platelet aggregation, but also increased the resistance of the myocardial cells to the injurious action of catecholamines.

Acute lesion of rat myocardium by a single injection of cobalt dichloride.

The formation of infarctoid areas in rat myocardium following intraperitoneal injection of cobalt dichloride (30 mg/kg) is connected with metabolic (toxic) and ischaemic lesions of myocardial cells. The ischaemic lesions are sequelae of thrombosis taking place after 3-8 hours in consequence of thrombocytic aggregation in the capillary lumen. With the aid of polarization and electron microscopy, the myocardial-cell changes in the affected zones were classed into four morphological types, as follows: contracture type, intracellular myocytolysis, primary clumpy disintegration of myofibrils, and intravital autolysis of ischaemized cells.