Uridine treatment prevents myocardial injury in rat models of acute ischemia and ischemia/reperfusion by activating the mitochondrial ATP-dependent potassium channel.

The effect of uridine on the myocardial ischemic and reperfusion injury was investigated. A possible mechanism of its cardioprotective action was established. Two rat models were used: (1) acute myocardial ischemia induced by occlusion of the left coronary artery for 60 min; and (2) myocardial ischemia/reperfusion with 30-min ischemia and 120-min reperfusion.

[Protective effect of uridine on metabolic processes in rat myocardum during its ischemia/reperfusion damage].

The experimental study of the cardioprotective effect of uridine, the metabolic precursor of the endogenous activator of mitochondrial ATP-dependent K+-channels (mitoKATP-channels), was performed using the model of myocardial ischemia/reperfusion (I/RP) in rats. Ischemia for 30 min followed by reperfusion for 120 min resulted in a significant decrease in ATP and phosphocreatine (PC) content, intensification of lipid peroxidation (LPO), and inhibition of the antioxidant system (AOS) in cardiomyocytes. Uridine in a dose of 30 mg/kg, administered intravenously prior to reperfusion, had a protective effect on myocardial metabolism in the I/RP zone.

[GLUCOSE CONTENT FLUCTUATION IN BLOOD OF NEWBORN RATS DEPENDING ON SEASON AND PATTERN OF SPONTANEOUS MOTOR ACTIVITY].

Earlier we have shown that in newborn rats the glucose level in blood serum changes depending on the pattern of spontaneous periodic motor activity (SPMA). During rest periods, both under dominant decasecond rhythm and under dominant minute rhythm, the glucose level in blood serum is higher than during activity periods. We have also shown that the glucose level in the blood serum rises with age reaching the level of adult animals by day 10.

Antiarrhythmic Activity of Taurepar during Ischemic and Reperfusion Damage to Myocardium.

The antiarrhythmic effect of taurepar, an N-phenylalkyl derivative of taurine, was examined in experiments on rats subjected to acute myocardial ischemia/reperfusion leading to arrhythmia development. During acute ischemia, taurepar (25 mg/kg) completely prevented early postocclusion arrhythmias including extrasystoles, ventricular tachycardia, and ventricular fibrillation. During postischemic reperfusion, taurepar (25 mg/kg) did not prevent extrasystoles and ventricular tachycardia, but precluded the development of ventricular fibrillation and the death of animals.

Antiarrhythmic effect of uridine and uridine-5'-monophosphate in acute myocardial ischemia.

Experiments on rats with acute myocardial ischemia accompanied by early postocclusive arrhythmias have shown normalizing, energy-stabilizing, and antiarrhythmic effects of uridine and uridine-5'-monophosphate. The drugs decreased lactate and restored reserves of glycogen and creatine phosphate depleted by ischemia. Uridine and uridine-5'-monophosphate significantly decreased the severity of ventricular arrhythmias.

Effect of uridine on energy metabolism, LPO, and antioxidant system in the myocardium under conditions of acute coronary insufficiency.

Experiments on rats have shown that preventive treatment with uridine stabilizes energy metabolism in the heart under conditions of 60-min left coronary artery occlusion. The preparation also prevented antioxidant system dysfunction and LPO hyperactivation. 5-Hydroxydecanoate, a selective blocker of mitochondrial ATP-dependent K(+)-channels, abolished the protective effect of uridine, which attested to the involvement of these channels into mechanisms of the cardioprotective effect of the preparation.

[The blood glucose content in newborn rats depending on level and pattern of spontaneous motor activity].

Earlier we have shown that administration to newborn rats of the pentose phosphate cycle inhibitor hydroquinone leads to a change in intensity and pattern of spontaneous periodic motor activity (SPMA) characteristic of early stages of development. The most typical was the disappearance of the rest period from the near-minute cycle "activity--rest" and the appearance of uninterrupted motor activity. In several cases, especially after 10 days of development, there was noted an enhancement in the SMPA pattern of the motor activity complexes following in the decasecond rhythm.

Comparative study of cardioprotective effects of uridine-5'-monophosphate and uridine-5'-triphosphate during the early periods of acute myocardial ischemia.

In experiments on rats, uridine-5'-monophosphate and uridine-5'-triphosphate reduced the intensity of anaerobic glycolysis and preserved glycogen stores and creatine phosphate balance during the first 60 min after occlusion of the left coronary artery. However, the energy-protective effect of uridine-5'-triphosphate developed 15 min later than the effect of uridine-5'-monophosphate. Uridine-5'-monophosphate, but not uridine-5'-triphosphate, reduced T wave amplitude on ECG and decreased the volume of ischemic injury to the myocardium.

Cerebroprotective effect of a new taurine derivative during cerebral ischemia.

A new taurine derivative chlorohydrate-N-isopropylamide-2-(1-phenylethyl)aminoethanesulfonic acid normalized energy metabolism, inhibited lipid peroxidation, and reactivated antioxidant enzymes in the brain of rats exposed to ischemia. This taurine derivative decreased the mortality rate of animals with ischemic changes in cerebral circulation. The test compound was more potent than piracetam in producing the cerebroprotective effect.

[The neuroprotector effect of a new taurine derivative on a model of compression spinal cord trauma in rats].

The neuroprotector effect of a new taurine derivative, 2-(1-phenylethyl)-aminoethanesulfonyl-2-propylamide hydrochloride, has been studied in rats with model compression spinal cord trauma. The drug favored restoration of the motor function of posterior extremities in rats with the model spinal cord trauma and significantly decreased the lethality in test animals. The taurine derivative normalized the energy metabolism, lipid peroxidation and antioxidant system in animals with spinal cord trauma.

Neuroprotective effect of cytoflavin during compression injury of the spinal cord.

Cytoflavin normalized energy metabolism, decreased the intensity of lipid peroxidation, and reactivated the antioxidant system in the spinal cord of rats with compression injury at the level of Th10-Th11. The neuroprotective effect of the test preparation manifested in normalization of hindlimb motor function and decrease in mortality rate of animals with spinal cord injury. Neuroprotective activity of cytoflavin was higher than that of Cerebrolysin.