[Post-resuscitation neurosomatic deviations and the feasibility of their correction with a drug of metabolic action]. / Postreanimatsionnye neirosomaticheskie otkloneniia i vozmozhnosti ikh korrektsii preparatom metabolicheskogo deistviia.

Circulation in white rat males was stopped for 10 minutes by ligation of the intrathoracic vascular bundle of the heart. Proxipin in a dose 10 or 20 mg/kg was injected i.p. after restoration of effective cardiac activity and the next 3 days. Proxipin improved resuscitation outcomes, relieved symptoms of CNS excitability 4-6 months after resuscitation, changed adaptation to stress agents, protected against risk-factors of atherogenesis. However, proxipin-induced inhibition of the motor activity suppressed the free-choice ability to find food.

[Effects of active behavior in the postresuscitation period on the functional and morphological characteristics of the brain]. / Vliianie aktivizatsii povedeniia v postreanimatsionnom periode na funktsional'nye i morfologicheskie kharakteristiki mozga.

Efficacy of prolonged (days 10-60 after resuscitation) regular activation of behavior by labyrinth training of 4-staged food search conditioned reflex is studied in rats subjected to 15-min circulation arrest. This training affected the function of the central nervous system, which manifested by decreased anxiety and a higher activity in the open field test. This functional exercise prevented fall-out of neurons in the fifth layer of hemispheres, of cerebellar Purkinje's cells, and of pyramidal neurons in hippocampal sector CA1. These results support the hypothesis proposed by A. M. Gurvich on the possibility of regulating the postresuscitation recovery of the central nervous system by neurophysiological treatment of the brain.

Prophylaxis of encephalopathies and risk factors of atherogenesis development in the postresuscitation period in rats by means of succinic acid.

The effect of oral administration of succinic acid was studied in 66 rats exposed to 10 min cardiac arrest with further resuscitation. A total of 30 mg/kg of the drug were administered daily for 5 days starting with day 3 up to day 7 after resuscitation. The experiments have revealed that treatment with succinic acid caused normalization of the orienting behavior in an 'open field' test, decrease of the intensity of response to electric shock, normalization of free radical formation in the brain and serum and reduced cerebral morphological changes. The succinic acid prevented the increase of cholesterol, triglyceride and low density lipoproteins in the blood. The data suggested that after additional trials the succinic acid could be used to prevent development of postresuscitation encephalopathies (3 months after reanimation).

[The effect of succinic acid on postresuscitation pathology of the CNS and of the body as a whole]. / Vliianie iantarnoi kisloty na postreanimatsionnuiu patologiiu TsNS i organizma v tselom.

The effect of oral succinic acid was studied in rats exposed to 10-min heart arrest followed by resuscitation. The drug was administered for 5 days in a dose of 30 mg/kg starting from day 3 up to day 7 after resuscitation. Succinic acid was found to normalize the orientation and exploration behavior of rats in the "open field" test, decreased the intensity of response to stress (electric shock), and normalized the radical formation in the brain tissue and blood serum, thus reducing the morphological changes in the brain. In addition, succinic acid prevented the development of risk factors of atherogenesis, namely, increase of the levels of blood cholesterol, triglycerides, and low and very low density lipoproteins. Further studies are needed to validate the addition of succinic acid to the armory of drugs preventing the development of postresuscitation encephalopathies in remote (3 months) periods.

[Post-resuscitation toxemia and possibilities of its correction by albosorb]. / Postreanimatsionnaia toksemiia i vozmozhnosti ee korrektsii al'bosorbom.

Albumin with enhanced sorption capacity (albosorb) was infused in animals after 10 min long clinical death caused by blood loss to correct endogenic intoxication. The albosorb infusion enhanced the blood plasma astringency both with respect to hydrophobic and hydrophilic molecules.

Rapid decrease of high affinity ouabain binding sites in hippocampal CA1 region following short-term global cerebral ischemia in rat.

High affinity [3H]ouabain binding was examined in the hippocampal CA1 region and frontal cortex of rats subjected to 5 min complete cerebral ischemia in a clinical death model, and to subsequent resuscitation. A decrease of Bmax directly after ischemia and its further gradual decrease during 120 min of reperfusion were noted in the ischemia-vulnerable CA1 region, whereas no change of Bmax was observed in frontal cortex. The apparent Kd constant showed insignificant fluctuations in either of the two brain regions. Since ouabain binds with high affinity to the neuronal (alpha +)-form of Na+/K+-ATPase, the results indicate a rapid enzyme loss in CA1 neurons. The high affinity ouabain binding test proved to be a sensitive detector of premorphological changes in nerve cell membranes in ischemia.

Ischemia modifies protein distribution in gerbil brain subcellular fractions.

This work deals with changes in sedimentation of proteins in subcellular fractions isolated from the ischemic brain of Mongolian gerbils. We analysed protein content and the activity of marker enzymes in P2, S2, M and S3 subfractions isolated after 10 min ischemia, ischemia combined with apnea or 1 h later, after recirculation. On the basis of protein balance, the distribution of marker enzymes and electrophoretic analysis of proteins in brain subfractions it was shown that in ischemia some fraction of proteins which are normally cytosolic and microsomal, cosediment with the crude mitochondrial pellet. This effect, aggravated in ischemia complicated by apnea, is reversible and after 1 h recirculation the protein distribution in the brain normalizes completely.

[Adenylate cyclase activity and cyclic AMP content in brain tissue of dogs during clinical death and in the post-resuscitation period]. / Aktivnost' adenilattsiklazy i soderzhanie tsAMF v tkani mozga sobak pri klinicheskoi smerti u v postreanimatsionnom periode.

The cAMP levels and adenylate cyclase activity have been studied in the grey brain substance and striatum system of dogs during circulation arrest due to electrotrauma of different duration (1-2, 15, 45 min) and in postresuscitation period in animals recovered after 15-min clinical death. Adenylate cyclase is strongly activated and cAMP levels are increased in the brain areas under study during complete brain ischemia. The cAMP levels in the grey substance and in striatum system are reduced considerably compared to the control, accounting for 12-20 on days 2-5 of postresuscitation period in animals with neurologic deficit. Adenylate cyclase and phosphodiesterase enzyme activity is twice higher in the striatum system and 50% lower in the grey brain substance than the baseline. The disturbances in cyclic nucleotide exchange, along with other factors seem to play an important role in the pathogenesis of postresuscitation encephalopathy.

[Membrane damage in brain subcellular structures in terminal states and in the postresuscitation period]. / Povrezhdenie membran subkletochnykh struktur golovnogo mozga pri terminal'nykh sostoianiiakh i v postreanimatsionnom periode.

Animal experiments were made to study and compare enzymatic activity of brain tissue mitochondria and microsomes treated and untreated with Tween-80 and Triton-X-100. In Mongolian gerbils, the 10-minute brain ischemia induced by bilateral carotid occlusion led to the labilization of the membranes of microsomal fractions, which did not return to normal an hour after resuscitation. The destructive effect of ischemia combined with clinical death from mechanical aspnyxia was similar to that of Triton-X-100. The ten-minute clinical death from ventricular fibrillation due to electroshock in dogs labilized lysosomal membranes. During the first hour after resuscitation and especially during the first 24 hours, the treatment of crude mitochondria with Tween-80 did not activate alkaline phosphatase and plasminogenic activator as compared with the control group.

[Change in the physicochemical properties of the cerebral cortical proteins in dying and resuscitation after mechanical asphyxia]. / Izmenenie nekotorykh fiziko-khimicheskikh svoistv belkov kory golovnogo mozga pri umiranii i ozhivlenii posle mekhanicheskoi asfiksii.

The physicochemical properties of protein postmitochondrial supernatant after gray substance of the brain homogenization undergo changes during clinical death caused by mechanical asphyxia. The shift on the densitogram occurs after protein electrophoresis in polyacrilamide gel. After sedimentation the total concentration of proteins and total activity of lactate dehydrogenase (LDH) decrease. Followiing adsorption on a DEAE-Sephadex A-50 the total fraction of nonadsorbed beta- and gamma-globulins also decreases, and the activity of LDH (3+4+5) isoenzymes falls significantly. Disturbed behavior pattern of proteins in the sedimentation and electrophoretic fields as well as changes in the sorption properties specific for varying times of clinical death, play a certain role in the development of irreversible changes in the gray substance of the brain. The adsorption and sedimentation properties of the proteins return to normal during early postresuscitation period, whereas the electrophoretic mobility of protein fractions in polyacrylamide gel remains unchanged within the first day.

[Effect of protracted infusions of polyglucin during the resuscitation period on metabolic and morphologic characteristics of the brain]. / Vliianie prodolzhitel'nykh infuzii poligliukina v postreanimatsionnom periode na metabolicheskie i morfologicheskie kharakteristiki mozga.

Polyglucine infusions (10 ml/kg) during the first 10 days of postresuscitation period after 4-hour hypovolemic hypotension promotes normalization of general RNA content, quick mobile protein fractions, corresponding prealbumins, albumins, postalbumins, ceruloplasmin, transferrin, and alpha-globulins. Macromolecular protein fractions beta- and gamma-globulins--remained considerably changed: beta-globulins doubled, and gamma-globulins decreased 1.7-fold. Acid phosphatase specific activity increased in the postmitochondrial supernatant by 53%; an increase in the acid phosphatase activity was revealed in the neurons, glia, and vascular endothelium. The amount of Purkinje's cells in the cerebral cortex in the experimental group did not differ essentially from the control values. Thus, the results obtained emphasize the importance of prolonged polyglucine infusions together with other resuscitation measures in the treatment of hypovolemic states.

[Posthypoxic changes in the cerebral cortex of dogs in the late recovery period after 4-hour hypovolemic hypotension]. / Postgipoksicheskie izmeneniia v kore golovnogo mozga u sobak v otdalennyi vosstanovitel'nyi period posle 4-chasovoi gipovolemicheskoi gipotenzii

On the 14th-21st day of the restorative period after four-hour hypovolemic hypotension the level of total RNA decreased in the tissue of the gray matter of the brain by 20.9%, and of DNA-by 13%. In the postmitochondrial supernatant the concentration of prealbumins was reduced by 26.5%, alpha-globulins--19.2%, gamma-globulins--by 59.8%; the concentration of albumins and beta-globulins was increased by 12.6% and 50.0%, respectively. The activity of acid cathepsins rose by 50%, and of acid phosphatase--by 44%. The activity of total lactic dehydrogenase (LDH) and glutamic dehydrogenase failed to differ essentially from the control level. However, LDH isoenzyme spectrum changes towards the reduction of LDH3+4+5 from 31.9 to 14.2%. Analysis of densitograms of electrophoresis in polyacrylamide gel showed physico-chemical changes in the protein molecules similar in nature to the denaturation phenomenon. The Purkinje's cell count decreased in the cerebellum by 41.3% in comparison with control.