In a rat model of 5-min clinical death caused by massive blood loss actovegin prevented the development of metabolic disorders induced by hypoxia and reoxygenation as well as the damage to the central nervous system in the early postresuscitation period. Intmcarotid administration of actovegin increased the activity of reduction-oxidation enzymes, intensified aerobic metabolism of glucose, prevented lactate accumulation in the brain, reduced structural disorders in the central nervous system, and provided lhster restoration of the major reflexes after a 5-min total ischemia. Key Words: central nervous system; postresuscitation period; actoveginFast and adequate restoration of the central nervous system (CNS) activity is an important resuscitation measure. Since the energy metabolism disorders are the major cause of postischemic damage to the brain [6,7], their timely normalization determines the course of postresuscitation period.In the present study we examined the effect of actovegin (AV), a deproteinated hemolysate which enhances aerobic metabolisln by intensifying the utilization of oxygen and glucose and stimulating ATP formation [9,10], on functional, metabolic, and morphological changes in the brain during postresuscitation period. MATERIALS AND METHODSExperiments were performed on outbred albino male rats (body weight 220-350 g) using a model of 5-rain clinical death caused by massive blood loss [81. Tracheostomy and catheterization of the common carotid artery were performed under Nembutal anesthesia (35 lng/kg intraperitoneally). The maximum possible volume of blood was relnoved through the catheter until cessation of respiration and heart beat and zero blood pressure in the carotid a1"te13r, which was considered as the beginning of clinical death. Resuscitation by the standard scheme was started after 5 rain. Artificial ventilation was performed throughout the entire postresuscitation period (40 min). Adrenomimetics were not administered.The rats were divided into 4 groups. Group I consisted of intact animals (n=14). Group 2 rots were subjected to 5-rain clinical death (n =14) without administering AV in postresuscitation period. Group 3 rats (n=Ig) were given AV in a total dose of 30 mg. In order to prevent sharp increase in energy metabolism the preparation was injected into the carotid m"tery in three equal doses on the 5th, 15th, and 30th rain of the postresuscitation period. Group 4 rats were administered an equivalent volume of normal saline (control, n=21).Arterial pressure and heart and respiratory rates were recorded before and on the 5th, 10th, 20th,

Hepatotoxicity of ozone in total systems treatment was evaluated by the functioning of hepatic oxidoreductases. Activities of lactate dehydrogenase and alcohol dehydrogenase were measured in liver homogenates of Wistar rats, injected daily with saline with saturating ozone concentrations of 3000, 10,000, and 40,000 μg/liter or placebo for 30 days. Systemic ozone treatment had a two-step effect on the hepatic oxidoreductases. Low doses (0.6 μg) promoted a moderate physiological stimulation of the enzymes, while in doses >2 μg ozone led to progressive tissue hypoxia and accumulation of toxic products in the liver.

We studied enzyme systems (lactate dehydrogenase) of mitochondria in cerebral nerve cells in experimental encephalopathy developing after thermal injury. In animals receiving neuromedin at the early terms after injury, the ratio of forward to reverse lactate dehydrogenase reactions significantly increased over the first day after injury and returned to normal on day 7.

Catalytical properties of aldehyde dehydrogenase were studied using preparations of this enzyme, obtained from control rats and rats with thermal injury. Aldehyde dehydrogenase was shown to participate in the metabolism of aromatic and aliphatic aldehydes. Kinetic characteristics of the enzyme with different substrates were studied under normal conditions and in thermal burn injury.

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We studied the kinetics of liver aldehyde dehydrogenase in rats with cold injury. Low-temperature exposure was followed by a decrease in activity and catalytic efficiency of aldehyde dehydrogenase in rat liver mitochondria. Atypical changes in kinetic characteristics of aldehyde dehydrogenase were found in the cytoplasmic fraction during cold injury.

A possible relationship between metabolic types of regulation of liver oxidative enzymes (lactate dehydrogenase and alcohol dehydrogenase) and the blood level of cortisol and insulin in intact animals is explored. The liver enzyme activity is found to depend on the initial physiological state of the organism.

Chorionic gonadotropin is shown to alter lactate dehydrogenase and alcohol dehydrogenase activity in the pathologically altered liver and to exert a regulatory effect on the catalytic properties of these enzymes. Key Words: chorionic gonadotropin; lactate dehydrogenase; alcohol dehydrogenase; liverOne approach to the management of chronic hepatitis and of cirrhosis consists in the use of agents that stimulate regeneration of the liver. It has been shown that chorionic gonadotropin (CG) stimulates liver regeneration and the reversal of pathological changes, with the result that the structure and function of this organ return toward normal [6]. CG promotes enhanced RNA synthesis and lowers the activity of lysosomal enzymes by elevating the activity of organ-specific enzymes (urokinase, fructose-l-phosphatase) [1,5]. Preliminary studies have indicated that CG has a direct effect on the catalytic properties of lactate dehydrogenase (LDH) in vitro [3], which suggests that this hormone may act as a nonspecific regulator of enzyme activity in the cell.The purpose of the present study was to examine how CG might affect the regulation of LDH and alcohol dehydrogenase (ADH) activity in the pathologically altered liver. MATERIALS AND METHODSThe effect of CG on LDH and ADH activity in the pathologically altered liver was studied on a model of toxic hepatitis produced in randomly bred male rats by administering them subcutaneously a 66% solution of carbon tetrachloride (CC14) in a dose of 0.3 ml 4 times per week over a 3-month period. After the discontinuation of CC14 injections, some of the rats were treated with CG and some were left untreated. CG was injected subcutaneously in a dose of 75 units per 100 g body weight. The animals were killed by decapitation 2 and 30 days after the start of hormone therapy. The control group consisted of intact rats. Activities of the direct and reverse LDH and ADH reactions were measured in liver homogenates and expressed in nrnol NADH/min per mg protein [4]. Table 1, the activity of the oxidative enzymes LDH and ADH was altered in the homogenates of livers from rats with toxic hepatitis. Thus, the activity of the direct LDH reaction was higher by 69% and that of the reverse LDH reaction lower by 40% than in the control group of intact rats. The activity of the direct and reverse ADH reactions was lower in both cases, by 51% and 55%, respectively. The reduced capacity of the liver to effect biotransformation of alcohols and aldehydes and the predominantly aerobic type RESULTS As shown in