[The effect of preliminary administration of dimethylsulfoxide on the development of experimental myocardial necrosis in rats treated with isoprenaline].

It has been suggested that in the genesis of isoprenaline-induced myocardial necrosis in rats, along with the intracellular calcium homeostasis and energy production breakdown, the mechanism of cytotoxic oxygen free radical generation is also included. The effects of dimethylsulphoxide, a hydroxyl radical scavenger, on the appearance of isoprenaline-induced myocardial necrosis in rats, were investigated. The verification of the efficacy of such pretreatment was based upon the monitoring of changes in plasma activity of enzymes creatine kinase, lactate dehydrogenase and alpha-hydroxybutyrate dehydrogenase, and upon the heart muscle sample light microscopy. The results have shown that the total plasma activity of all the observed enzymes was six hours after isoprenaline application several times increased, as compared with the control values. Histopathological changes in unprotected animals were evident and consisted of coagulation necrosis and myocytolysis. In both dimethylsulphoxide and isoprenaline treated groups of rats only a statistically insignificant increase in enzyme plasma activity was observed, while heart histopathological changes showed considerable reduction both in extensity and intensity of the tissue damage. The evident efficiency of dimethylsulphoxide in the prevention of the extent of myocardial necrosis in rats after the administration of the toxic dose of isoprenaline suggests that the generation of hydroxyl anion radicals, probably via autooxidation of isoprenaline, is a possible mechanism of the tissue injury in this experimental model.