[Precursors of histidine-containing dipeptides in the muscle tissue of invertebrates].
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Biomedical subjects
Publications and source records attributed to A V Lebedev.
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The effect of two methyluracil forms on the composition of lipids, the content of peroxidation products and the amount of lipid-soluble scavengers of free radicals was studied in rat liver and heart tissues. Both these forms caused an increase in content of total lipids in the animal liver tissue 2 hrs after injection, whereas beta-form increased 1.6-fold the content of cholesterol esters and 1.9-fold that of triglycerides in liver tissue, unlike the alpha-form which affected these parameters slightly. The effect of methyluracil polymorphic derivatives on lipid peroxidation (TBA-positive products) was not detected. The methyluracil beta-form, not affecting the total pool of hydrophobic antioxidants, was found to decrease the content of active scavengers of free radicals in rat liver and heart tissues, as well as beta-form decreased the content of vitamin E in these tissues. At the same time, the methyluracil alpha-form did not affect the composition of tissue hydrophobic antioxidants. These differences found in the effect of two methyluracil forms on lipid composition and lipid-soluble scavengers of free radicals may be responsible for biological nonequivalence of the drug polymorphic forms.
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The effect of the antioxidant histochrom on the size of the myocardial infarction and activity of the cardioselective enzyme creatine phosphokinase was studied in 45 patients with acute myocardial infarction during thrombolytic therapy. Changes in blood plasma histochrom concentration were studied in 7 patients with myocardial infarction after a single intravenous infusion of 100 mg of the drug. The pharmacokinetic parameters of the drug are shown. The use of histochrom in thrombolytic treatment of acute myocardial infarction lead to limitation of the necrotic zone and increase of myocardial contractility, and results in a more favorable course of the processes of left-ventricular remodeling.