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.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.