Effect of chronic alcohol consumption on the myocardial microcirculatory bed

Abstract

Experiments were carried out on male Wistar rats weighing 150-180 g. All animals of the experimental groups were given ethanol for 12 weeks in a dose of 36% of the total calorific value of the diet, mixed with semisolid food [6]. Animals of the first group also were given an intraperitoneal injection of the specific catalase inhibitor, 3-amino-l,2,4-triazole, in a dose of i g/kg on alternate days to create a model of experimental ACMP [3, 6]. The animals of group 2 also received ethanol but on alternate days they were given an intraperitoneal injection of physiological saline (control to group i). The rats of group 3, unlike those of group i, received vitamin E in excess of its amount in the diet daily in a dose of I mg/kg to correct changes arising in ACMP. Animals of groups 4 and 5 were given another antioxidant, dibunol (4-methyl-2,6-di-tert-butylphenol) in doses of i00 and i0 mg/kg respectively for the same purpose. The control animals of group 6 received a diet of the same calorific value as the groups receiving ethanol, as a result of the addition of sucrose to the diet. In each group five animals were investigated. After decapitation of the rats the heart was removed and kept in cold isotonic potassium chloride solution. Material from the left ventricle was prepared for electron microscopy as described previously [3], including electron-histochemical detection of nickel as a marker of myocardial anoxia [4], and the method with colloidal lanthanum to determine membrane permeability [7].