Study of the Cardioprotective Properties of Uridine-5'-Monophosphate and Uridine in a Rat Model of Myocardial Damage Induced by Isoprenaline

The effects of uridine and its monophosphoryl derivative both on the level of the main biochemical markers of myocardial damage in the blood and the electrical activity of the heart were investigated in a rat model of cardiomyopathy induced by isoprenaline. It was shown that the administration of isoprenaline (150 mg/kg, subcutaneously) caused an increase in the activity of serum enzymes aspartate aminotransferase (AST) and alanine aminotransferase (ALT), leading to the elevated AST/ALT ratio or De Ritis ratio, and enhanced activity of lactate dehydrogenase in blood lymphocytes, which confirms the development of myocardial damage in experimental animals. ECG analysis has revealed prolonged RR, P-R, QT, QTc intervals and QRS complex, which indicates that the duration of depolarization and repolarization phases increases relative to the duration of the cardiac cycle in rats with isoprenaline-induced myocardial damage. Preliminary administration of uridine and uridine-5'-monophosphate to experimental animals at a dose of 30 mg/kg equally effectively prevented an increase in the enzymatic activity of AST and the De Ritis ratio, led to a decrease in the duration of P-R, QRS, QT and QTc intervals as well as to partial normalization of metabolic activity of rat blood lymphocytes. These findings suggest that uridine and uridine-5'-monophosphate have a similar protective effect on the contractile function of cardiomyocytes and can be used as agents for metabolic therapy in the treatment of ischemic heart disease.