Injury to membranes of subcellular brain structures in terminal states and in the postresuscitation period

Molchanova, L. V.; Pylova, S. I.; Zaks, I. O.

doi:10.1007/bf00834171

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“…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.…”

Section: Abstract: Central Nervous System; Postresuscitation Period;mentioning

confidence: 99%

Effects of actovegin on the central nervous system during postischemic period

et al. 1998

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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,

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“…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.…”

Section: Abstract: Central Nervous System; Postresuscitation Period;mentioning

confidence: 99%