[The synthesis of phosphates of long-chain omega-hydroxyalkyl esters of 11-deoxyprostaglandin E1].

Di(p-methylbenzyl) phosphates of omega-hydroxyalkyl esters of 11-deoxyprostaglandin E1 were synthesized from disubstituted 1,10-decane and 1,22-docosane derivatives for studying permeability of bilayer membranes. The English version of the paper.

[The effect of mildronate on carnitine-dependent and carnitine-independent ketogenesis in rats].

Mildronate of 3-(2,2,2-trimethylhydrozinium)propionate, a novel anti-ischemic drug, inhibits the biosynthesis of carnitine from Y-butyrobetaine. Continuous administration of mildronate (200, 400 mg/kg for 10 days orally) to rats exerted a marked antiketogenic action on the animals deprived of food for 48 hours. In the fed rats receiving sodium octanoate a course treatment with mildronate elevated to concentration of ketone bodies in blood serum.

[The effect of a structural analog of gamma-butyrobetaine, mildronate, [3-2,2,2-trimethylhydrazine)propionate] on dynamic carnitine-dependent metabolism].

Inhibitor of carnitine-dependent metabolism mildronate, 3-(2,2,2-trimethylhydrazinium) propionate, administered into rats at a dose of 200 mg/kg, per os, within 10 days, caused a decrease in concentration of free carnitine and of long-chain acylcarnitine in myocardium as well as contributed to accumulation of free fatty acids in blood serum. Besides, the rate of I-14C-palmitic acid turnover to 14CO2 was decreased in myocardium homogenate. The drug inhibitory effect on carnitine biosynthesis from gamma-butyrobetaine was responsible for the phenomenon observed.

[Potentiation of the antiketogenic effect of exogenous glucose with the help of the new beta-oxidation inhibitor mildronate--3-(2,2,2-trimethylhydrazine)propionate].

Antiketogenic effect of exogenous glucose (2 g/kg, per os, 1 hr before death) was potentiated after preadministration of mildronate 3-(2,2,2-trimethylhydrazinium) propionate into rats either kept on usual ration or fasting within 48 hrs at a dose of 200 and 400 mg/kg, per os, during 10 days. Mildronate is inhibitor of carnitine-dependent metabolism of fatty acids affecting at the step of gamma-butyrobetaine turnover into carnitine. The drug inhibitory influence studied appears to be realized via activation of the glycolytic pathway of glucose metabolism specific for inhibitors of beta-oxidation.

[Study of the effect of an inhibitor of carnitine-dependent metabolism of mildronate on the oxidation of fatty acids in the liver mitochondria of intact rats].

Effect af antiischemic drug mildronate 3-(2,2,2-trimethylhydrazinium) propionate on oxidation of sodium octanoate and L-palmitoyl carnitine was studied in liver mitochondria of intact rats using polarographic procedure. After 10 days of administration of mildronate at a dose of 200 mg/kg per os oxidation of sodium octanoate was stimulated in liver mitochondria while the rate of L-palmitoyl carnitine oxidation was unaltered. The data obtained suggest that mildronate stimulated the carnitine-independent fatty acid oxidation which appears to occur as a compensation for inhibition of the carnitine-dependent oxidation by the drug.