Trimetazidine has an antianginal, antihypoxic effect. Directly affecting the cardiomyocytes and neurons of the brain, it optimizes their metabolism and function. The cytoprotective effect is caused by an increase in the energy potential, activation of oxidative decarboxylation, and rationalization of oxygen consumption (increased aerobic glycolysis and fatty acid oxidation blockade). Supports contractility of the myocardium, prevents the decrease in intracellular content of ATP and phosphocreatinine. In conditions of acidosis normalizes the functioning of membrane ion channels, prevents the accumulation of calcium and sodium in cardiomyocytes, normalizes the intracellular content of potassium ions.Reduces intracellular acidosis and phosphate content due to myocardial ischemia and reperfusion. It prevents the damaging action of free radicals, preserves the integrity of cellular membranes, prevents activation of neutrophils in the ischemic area, increases the electric potential decreases the yield of creatine from the cells and the severity of ischemic myocardial injury.
When the frequency of attacks of angina reduces (decreases nitrate consumption) after 2 weeks of treatment increases exercise capacity, reduced blood pressure drops. The hearing and results of vestibular samples in patients improve, dizziness and tinnitus decrease.
In vascular pathology, the eye restores the functional activity of the retina.