Cytoflavin normalized energy metabolism, decreased the intensity of lipid peroxidation, and restored activity of the antioxidant system in rat brain during postischemic reperfusion. Cerebroprotective effect of cytoflavin was similar to that of piracetam.
Key Words: cytoflavin; piracetam; ischemia; postischemic reperfusionHypoxia plays the major role in the pathogenesis of acute ischemic damages to cerebral blood flow. Hypoxia triggers the cascade of metabolic transformations modulating the intensity of energy metabolism and lipid peroxidation (LPO) [1,8]. Therefore, the therapy of acute cerebral ischemia should include not only correction of cerebral blood flow with vasoactive, fibrinolytic, and antiaggregant agents, but also normalization of energy metabolism and stabilization of cell membranes and subcellular structures in nerve cells.Here we studied effects of cytoflavin on brain metabolism during postischemic reperfusion damage. Cytoflavin (Polysan) is a complex preparation containing succinic acid, purine nucleoside (riboxine), nicotinamide, riboflavin mononucleotide, and N-methyl-D-glucamine (solubilizer).
MATERIALS AND METHODSExperiments were performed on 100 male outbred albino rats weighing 180-200 g (Rappolovo nursery). Ischemic brain damage was induced by 90-min occlusion of the common carotid arteries followed by repeffusion. The effect of cytoflavin (1.5 ml/kg) on postischemic brain damage was examined 24 and 72 h after reperfusion. The effects of cytoflavin were comDepartment of Neuropharmacology, Institute of Experimental Medicine, Russian Academy of Medical Sciences; Polisan Research-andProduction Pharmaceutical Company, St. Petersburg pared with those of piracetam (100 mg/kg). Control animals received an equivalent volume of physiological saline. The preparations were injected intraperitoneally 2 times a day. Control group comprised shamoperated rats.Energy metabolism in brain tissue was evaluated by the content of lactate and pyruvate [15] and lactate dehydrogenase (LDH) and succinate dehydrogenase (SDH) activities [5,6]. The intensity of LPO was estimated by the concentrations of malonic dialdehyde (MDA) and conjugated dienes (CD) of unsaturated fatty acids [12,13]. The state of the antioxidant system was analyzed by superoxide dismutase (SOD) activity and content of reduced glutathione (GSH) [3,11].-The results were analyzed by Student's t test.
RESULTSThe content of lactate and LDH activity in rat brain after common carotid artery occlusion increased by 194 and 107%, and pyruvate concentration and SDH activity decreased by 54 and 51%, respectively, compared to the control (Table 1). The lactate/pyruvate ratio reflecting the intensity of aerobic or glycolytic carbohydrate metabolism increased from 8.6 to 55.4. These data indicated inhibition of aerobic and stimulation of glycolytic (emergency) mechanisms of energy formation. The intensity of LPO increased, and the antioxidant system was suppressed in the ischemic brain. The 0007-4888/00/0002-128525.00 9Kluwer Academic/Plenum Publishers Metabol...
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.
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 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.
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.
Hepatoprotective effect of a diet containing soybean proteins most pronounced in soybean milk was demonstrated on the model of chronic toxic hepatitis. Results of biochemical studies correlate with morphological data indicating that soybean proteins hold much promise for supportive therapy of patients with chronic liver diseases.
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