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. The antiarrhythmic potency of taurepar surpassed that of lidocaine during acute myocardial ischemia and that of propranolol during ischemia/reperfusion injury. The results suggest that taurepar is a promising antiarrhythmic drug with high antifibrillation activity.

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. Both drugs reduced the incidence and duration of fibrillation. Uridine -5'-monophosphate demonstrated most pronounced antifibrillatory effectiveness. We hypothesize that the antiarrhythmic effect of the drugs is determined by their capacity to activate energy metabolism.

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.

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.

[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. The neuroprotector effect of the new taurine derivative significantly exceeds the action of cerebrolysine.

[Antiamnesic effect of cytoflavin and neuronol in rats with ischemic impairment of cerebral circulation]. / Antiamnesticheskii éffect tsitoflavina i neironola pri ishemicheskom narushenii krovoobrashcheniia u krys.

The antiamnesic action of the new complex preparations cytoflavin and neuronol was studied in rats with a cerebral ischemia model, tested for the passive avoidance conditioned reflex. The neuroprotector effect of drugs was determined by morphological methods. Both cytoflavin and neuronol reduced neuronal damage in the pyramidal layer of the hippocampus and prevented the development of amnesia during the entire period of cerebral ischemia (3-21 days). Both drugs also improved horizontal locomotor activity and emotional reactions of animals in the open field test.

Effects of cytoflavin and neuronol on morphological changes in the brain and survival of rats with ischemic disturbances in cerebral blood flow.

Cytoflavin and neuronol produce vasoactive and neuroprotective effects in rats with cerebral ischemia. Vasoactive activity of neuronol was higher than that of cytoflavin. These differences were most pronounced at the level of microcirculation. Test preparations were equally potent in producing the neuroprotective effect. Cytoflavin and neuronol markedly decreased the mortality rate of animals. Over the first 6 h of ischemia the relative effectiveness of cytoflavin was higher than that of neuronol. However, neuronol exceeded cytoflavin in the relative effectiveness during the follow-up period (days 1-21).

[Neuroprotective effect of cytoflavin in closed craniocerebral trauma]. / Tserebroprotektivnyi éffekt tsitoflavina pri zakrytoi cherepno-mozgovoi travme.

The efficacy of a complex preparation cytoflavin was studied on rats with a model of closed craniocerebral trauma. Cytoflavin produced normalization of the energy exchange, lipid peroxidation, and antioxidant system functioning in nervous tissues. The treatment significantly reduced the degree of posttraumatic edemation in the brain. The cerebroprotective action of cytoflavin was somewhat superior to the effect of the reference drug solcoseryl.

[Use of cytoflavin for correction of complications of myocardial infarction]. / Ispol'zovanie tsitoflavina dlia korrektsii posledstvii ishemicheskogo povrezhdeniia miokarda.

The possibility of using a combined preparation cytoflavine was studied on rats with myocardial infarction induced by coronary artery occlusion. The drug produces a positive action upon the energy exchange and the lipid peroxidation process and normalizes functioning of the system of antioxidant protection of the ischemized myocardium. Cytoflavine treatment led to a more favorable course of ischemic and necrotic processes and optimum organization of the necrosis zones.

[Therapeutic effects of a new taurine derivative in chronic hepatic diseases]. / Issledovanie terapevticheskikh svoistv novogo proizvodnogo taurina pri khronicheskoi patologii pecheni.

Therapeutic properties of a novel taurin N-phenylakyl derivative (TAU-15) in a dose 25 mg/kg were studied in male rats on models of chronic toxic hepatitis and partial hepatectomy. A hepatoprotective action of TAU-15 was established which is due to antioxidative action of TAU-15 and its ability to normalize protein-synthetizing activity of hepatocytes.

[Effect of the novel taurine derivative on various parameters of metabolism on experimental myocardial infarction]. / Izuchenie vliianiia novogo proizvodnogo taurina na nekotorye pokazateli metabolizma pri éksperimental'nom infarkte miokarda.

The effects of TAU-5, a new N-phenylalkyl derivative of taurine, on the metabolic changes in heart were studied in rats with experimental myocardial infarction. The new drug exhibits a pronounced antiischemic effect related to recovery of the activity of enzymes involved in the energy exchange, decrease in the rate of lipid peroxidation, and normalization of the function of enzymes responsible for the antioxidant activity. The results of the pathomorphologic analysis and data on the state of cardiac metabolism showed that the antiischemic effect of TAU-5 is comparable with that of neoton.

[Cycloferon in treating duodenal ulcers in rats]. / Tsikloferon v terapii iazvy dvenadtsatiperstnoi kishki u krys.

The possibility of using cycloferon (interferon inductor) for a complex treatment (in combination with the main drug solcoseryl possessing pronounced therapeutic properties) of duodenum ulcers was experimentally studied in male rats. The experiments showed a considerable difference in the interferon status of animals with model duodenum ulcers treated with cycloferon, solcoseryl, their combination, and placebo (control). The healing effect of solcoseryl administered in combination with cycloferon exceeded that of each component administered separately.

[Experimental evidence for pharmacotherapy of cardiovascular and gastroduodenal diseases induced by the body's extreme exposures]. / Eksperimental'noe obosnovanie farmakoterapii serdechno-sosudistoi i gastroduodenal'noi patologii, vyzvannoi ékstremal'nymi vozdeistviiami na organizm.

The results of examining the mechanisms of development of neurogenic visceral abnormalities induced by the body's extreme exposures, search for modes of its pharmacological correction are presented. Experiments have provided evidence for that the neutropic agents recovering the functional activity of the sympathetic nervous system, normalizing energy and plastic exchange have a positive effect in the treatment of the cardiovascular and gastroduodenal diseases which are caused by a neurogenic agent. A basically new approach to treating peptic ulcer, coronary heart diseases, and myocardial infarction is proposed depending on the stage of a disease.

[Central mechanisms of neurogenic gastric lesion and its pharmacologic correction]. / Tsentral'nye mekhanizmy razvitiia neirogennogo povrezhdeniia zheludka i ego farmakologicheskaia korrektsiia.

The study was undertaken to study the central mechanisms responsible for the development of neurogenic gastric lesion caused by a concurrent action of immobilization and 3-hour electrostimulation. With this action, there was a reduction in the levels of norepinephrine, dopamine, and GABA and impaired energy formation processes in brain tissue. Prior administration of L-DOPA, aethimizolum, phenibutum, and piracetam prevented changes in neurotransmitter balance and nerve tissue energy exchange. The drugs under study had positive preventive and therapeutical effects in experimental gastric lesions.