[The effect of the carnitine biosynthesis inhibitor mildronate on the lipid metabolic indices of rats]. / Vliianie ingibitora biosinteza karnitina mildronata na nekotorye pokazateli lipidnogo obmena u krys.

The course administration of a carnitine biosynthesis inhibitor mildronate (100 mg/kg, orally, for 10 and 30 days) was shown to increase the rat blood serum concentration of free fatty acids. By the 30th day of the treatment no changes in the rat myocardium contents of free fatty acids, triglycerides and cholesterol were found that along with the prevention of the accumulation of long chain metabolites of fatty acids in the heart under conditions of adrenergic actions indicated the pathogenetically right approach to the treatment of ischemic heart disease with mildronate.

[Effect of the calcium antagonists ryodipine and verapamil on the carnitine-dependent metabolism of fatty acids in the rat heart]. / Vliianie antagonistov kal'tsiia riodipina i verapamila na karnitinzavisimyi metabolizm zhirnykh kislot v serdtse krys.

Riodipine (10 days, 10 mg/kg) was shown to prevent in rats an isoproterenol-induced increase of free fatty acid concentration in the blood serum and heart and to promote normalization of long-chain acylcarnitine content in the heart. Under the same conditions verapamil caused an increase in free acid concentration in the blood serum and prevented their accumulation in the heart. Its ability to limit accumulation of long-chain acylcarnitine manifested itself in a lesser degree as compared to riodipine. Riodipine exerted no effect on oxidation of 1-14-C-palmitic acid by the rat heart homogenate, verapamil suppressed oxidation of this fatty acid.

[Biochemical effects of ryodipine (foridon)--a new calcium antagonist and derivative of 1,4-dihydopyridine]. / Izuchenie biokhimicheskikh éffektov riodipina (foridona)--novogo antagonista kal'tsiia, proizvodnogo 1,4-digidropiridina.

Ryodipine (foridon)--2, 6-dimethyl-3,5-dicarbomethoxy-4-(o-difluoromethoxyphenyl)-1, 4-dihydropyridine--similarly to nifedipine but at a lesser degree than nicardipine causes an increase of cAMP concentration in the slices of the rabbit myocardium and aorta. This property of 1,4-dihydropyridines is reflected in their effect on the uptake of 45Ca2+ by the myocardial strips. In the range of concentrations of 10(-4)-10(-6)M inhibition of 45Ca2+ transport is enhanced with a decrease of concentrations of the drugs. Under inactivation of potential-dependent transport of Ca2+, 1,4-dihydropyridines enhance the uptake of 45Ca2+. The similar effect was found at incubation of the myocardial slices in a polarizing buffer (2.68 mM K+). Verapamil, irrespective of the degree of depolarization (60,123 mM K+), suppressed in a linear dependence the uptake of 45Ca2+ and failed to influence this process in the absence of potential-dependent transport of Ca2+. By its biochemical effects ryodipine does not differ from the known derivatives of 1,4-dihydropyridine but has, like nifedipine and nicardipine, significant differences as compared with verapamil.