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Purpose. To study the effect of hyperbaric oxygenation (HBO) on the oxygen regime and ammonia metabolism in the neurons of cat cortex in hemorrhagic shock.Material and methods. Experiments were performed on 164 cats (males). The effect of HBO (3 ATA, 50 min) on cerebral blood flow (CBF), oxygen tension (PO2), the content of ammonia (Am), glutamine (Gn), glutamate (Gt), α-ketglutarate (α-KG), the activity of glutamate dehydrogenase (GDG), glutamine synthetase (GS), phosphate-dependent glutaminase (PDG) activity was studied in the sensorimotor cortex (SMC); the content of Am, GN and oxygen parameters in arterial (AB) blood and venous blood (VB) of the sagittal sinus in hemorrhagic shock caused by fractional bloodletting of their femoral artery at a rate of 10ml/kg/10 min in an average volume of 24±0.8 ml/kg, which was stopped with a decrease in systolic blood pressure to the level of 60.0±1.5 mm Hg. HBO was commenced on post-hemorrhagic minute 10 following the regimen of 3 ATA for 60 min.Results. The decrease in CBF and PO2 in SMC develops as early as the 10th minute of hemorrhagic shock, progressing to the stage of hemorrhagic shock decompensation (60±14 min). Accumulation of Am in the SMC at the stage of hemorrhagic shock decompensation associated with stimulation of PDG and GDG activity, inhibition of hemorrhagic shock activity and deficiency of α-KG. HBO, without eliminating hypoxia in SMC, prevented the development of the decompensation stage in animals with GS, pathological accumulation of Am, and a decrease in the activity of hemorrhagic shock. HBO increases the Gn increment from the SMC, into the blood. Under HBO conditions, the stimulating effect of hypoxia on GDG activity remains, but the concentration of glutamate remains within the normal range, as does the activity of PDG.Conclusion. Hyperbaric oxygenation, without eliminating hypoxia in SMC, which develops in hemorrhagic shock, prevents a violation of the exchange of ammonia in it, caused by acute non-compensated blood loss.

Material and methods. The studies were performed on 75 white mature rats (females) weighing 180—220g. Partial hepatectomy was performed by resection of a part of the left lobe of the liver (15—20% of the organ weight). Hyperbaric oxygenation (HBO) was performed three times (3 ata, 50 min). The first, second and third sessions were performed 4—8 hours, 24 hours and 48 hours after the surgery, respectively. The urea level was determined in the tissues of visceral organs, as well as in arterial blood (aorta), portal blood, blood from renal and hepatic veins, bile from common bile duct, and in urine on the 1st, 4th and 11th days of posthyperoxic period (days 3, 7 and 14 post-surgery).Results. Activation of the urea incretion from the operated liver to the bloodstream under hyperoxic conditions was accompanied by increased urea concentration in the arterial blood and excretion from the body with urine that was facilitated by the elimination of a stimulating effect of PHE on the reabsorption of urea in the kidneys by the HBO procedure. At the same time, the production of urea in the renal tissue was activated and further released to the circulation through the renal vein. Stimulation of the liver and intestinal urea circulation by HBO was accompanied by the preservation of the stimulating effect of PHE on its accumulation in duodenum and colon tissues. In the thyroid gland, spleen, heart, and lungs of operated rats, HBO activated the transition of the «arterial» urea from the free form to the bound one. Termination of HBO normalized the urea concentration in the arterial blood by the 11th day of the posthyperoxic period whereas urea continued to be accumulated the heart, spleen, lungs, and intestine. A preserved increased release of urea from the operated liver into the bloodstream after HBO was accompanied by partial retention in the hepatocytes of urea delivered via bloodstreem through the portal vein. On the 11th day after HBO, the repeated hyperoxic activation of the liver and intestinal urea circulation occured, as well as HBO-restored stimulation of its production in the kidneys resulted in urea release into the renal vein and excretion with urea.Conclusion. HBO provides a correcting effect on alteration of circulating urea caused by PHE.

Purpose. To study glutamate metabolism characteristics in phylogenetically different parts of the mammalian brain in experimentally induced hemorrhagic shock (HS) in cats.Material and methods. Experiments were performed on 76 cats. HS was induced by intermittent bloodletting from femoral artery at a rate of 10ml/kg•10 minutes, with the average volume of 24±0.8 ml/kg. The bloodletting was discontinued after arterial pressure (BP) drop to 60.0±1.5 mmHg. We studied ammonia, glutamate (Gt), and α-ketoglutarate (α-KG) levels and glutaminase (GS) and glutamate dehydrogenase (GDG) activity in specimens harvested from phylogenetically different parts of the brain (cortex, limbic system, diencephalon, and medulla oblongata).Results. In intact animals, the peak GDG activity was found in the medulla oblongata (phylogenetically the oldest part of the brain) and the peak GS activity was registered in the sensorimotor cortex (phylogenetically the youngest part of the brain); the glutaminase activity did not depend on the phylogenetic age of brain structures.In the case of HS, Gt metabolism changes began in the sensorimotor cortex manifested by decreased GS activity, which progresses by the 70th minute of the post%hemorrhagic period (PHP) accompanied by delayed increase in the GDG and glutaminase activity, as well as Gt accumulation. In the limbic system and diencephalon the Gt metabolism was changing (impaired glutamine synthesis, stimuled Gt synthesis with glutamine desamidization and α%KG amination) when developed by the 70th minute of the PHP. Similarly to sensorimotor cortex, changes were associated with Gt accumulation. During the agony, α%KG deficiency developed in all parts of the brain as a result of its increased contribution to Gt synthesis. At the same period of time, in the sensorimotor cortex, limbic system and diencephalon the Gt synthesis from glutamine was stimulated, however, the Gt contribution tothe formation of glutamine was decreased. The accumulation of ammonia regardless of the HS stage was detected only inthe sensorimotor cortex, limbic system and diencephalon; in the medulla oblongata ammonium increase was found only during the agony.Сonclusion. HS creates conditions for glutamate accumulation in nerve cells by impairing the metabolism of glutamate in the brain structures. The nature and scope of these disorders depend both on the intensity of glutamate metabolism in phylogenetically different brain structures in acute blood loss and HS.

Purpose. To study urea kinetics in the body after liver resection in the experiment.Material and Methods. Experiments were carried out on 45 white female rats weighing between 180 g and 220 g. Liver resection (LR) was performed under ester anesthesia, wherein 15—20% of the organ weight was removed. Urea content was studied in biological fluids (arterial blood, venous — v.porta, v.hepatica, v.renalis — blood, choledochal bile, urine), and tissues of visceral organs (the thyroid gland, lungs, heart, liver, kidneys, spleen, stomach, intestine) on days 3, 7, and 14 after LR. Results. LR, while reducing the urea content in the v. hepatica blood, does not lead to similar changes in the arterial blood. This is accompanied by increased urea reabsorption in kidneys and higher v.porta blood urea content, which, depending on the postoperative time, results either from reduced urea excretion into the small intestine lumen or from its greater production by enterocytes followed by metabolite intake into the portal blood flow. The urea intake from hepatocytes into the hepatic bile ducts did not change on day 3 after LR; however, it increased on day 7 and slowed down on day 14. LR caused no changes in the gastric tissues urea content; never theless, it led to its increased content in the duodenal and colonic tissues. Without affecting the cardiac muscleurea content, LR entailed its increase in the lungs and thyroid gland on postoperative days 3, 7, and 14. At the background of absence of similar changes in the arterial blood data indicates promotion of urea production by the cells of these organs or metabolite retention therein.Conclusions. LR not only changes urea kinetics in the portal system organs, but also activates extrahepatic mechanisms aimed at preventing development of the arterial blood urea deficit because of its abnormal intake from the resected organ into the central blood flow.

Objective: to study the impact of hyperbaric oxygenation (HBO) on renal ammonia excretion during liver resection (LR). Material and methods. Experiments were carried out on 138 pubescent rats (females). Three HBO sessions were performed at 3 ATA lasting 50 min once daily after LR (15—20% of the liver weight). The kidney, blood (aorta, v. renalis), and urine were examined. The levels of ammonia, glutamine, and urea were measured. Results. By eliminating postoperative arterial hyperammonemia, HBO stimulates urinary ammonia ion excretion. This is achieved through elimination of the inhibitory effect of LR under HBO on ammonia secretion into the renal tubules and through activation of intracellular ammoniagenesis in nephrocytes, including that uncoupled with arterial glutamine deamidation. HBO potentiates simultaneously the activating effect of LR on the glutamine cycle in the kidneys mainly through the hyperproduction of renal glutamine and its influx from them into the bloodstream. HPO enhances the stimulatory effect of LR on urea reabsorption in the kidneys, but, unlike non-oxygenated rats, there was no reduction in urine urea excretion due to increased arterial blood urea concentrations. Termination of the body's exposure to hyperoxia restores urea reabsorption in the kidneys with the persisting stimulatory impact of HBO on the formation of urea by nephrocytes and its incretion from the latter into the bloodstream.

Objective: to study the anticolibacillary activity of arterial (aorta) and venous (portal vein, hepatic veins) blood during hepatectomy and hyperbaric oxygenation (HBO).Material and methods: Experiments were conducted on 40 non-inbred female albino rats exposed to hepatic resection (15—20% of organ mass) and HBO at 3 ata for 50 min once daily within the first three days after surgery. The bactericidal action of blood serum against E.coli and the capacity of neutrophils and monocytes to absorb this microbe were investigated.Results: HBO prevents a hepatectomy-induced reduction in serum bactericidal activity in the portal venous blood, but its reduction in arterial blood remains. Along with this, hepatectomy-induced impairment in the capacity of the liver to stimulate the phagocytic activity of neutrophils and monocytes against E.coli is eliminated under HBO. The latter selectively stimulates the rate of venous blood neutrophilic absorption of E.coli, with this property being lowered in monocytes.Conclusion: HBO eliminates the body’s anticolibacillary defense impairments during hepatectomy.

Objective: to examine nitrogen metabolism in the organs of the portal system during liver resection (LR) and hyperbaric oxygenation (HBO).Material and methods: Experiments were conducted on 65 female albino rats. LR was made under ether anesthesia, by removing a portion of the left hepatic lobe with an electric knife, which amounted to 15—20% of the organ’s mass. HBO was performed using medical oxygen at 3 ata for 50 min once daily within the first three days after LR. Lung tissue, gastrointestinal tract (GIT), spleen, and choledochal bile were the subject of the study. The tissue and blood levels of ammonia, glutamine, and urea were measured.Results: LR leads to pathological ammonia accumulation and decreases arterial glutamine consumption in GIT organs. Concurrently, the urea contained in the organs begins to come into portal blood flow, splenic glutamine deficiency develops, and hepatic ammonia-absorptive, glutamine- and urea-excretory functions diminish. Post-LR HBO prevents the accumulation of ammonia in the liver and GIT, restores the ammonia-absorptive, glutamine- and urea-excretory functions of the liver, and stimulates its glutamine and urea accumulation. Concomitantly, under HBO, there is an increase in glutamine entrance from the GIT into blood flow, but there is a decrease in GIT urea excretion and portal venous blood ammonia levels. HBO eliminates arterial hyperammonemia after LR and splenic glutamine deficiency.Conclusion: Hyperbaric oxygen eliminates nitrogen metabolic disturbances in the portal system, regulates compensatory-adaptive ammonia metabolic reactions triggered in the GIT and spleen during LR.

Objective: to study the impact of liver resection (LR) and a hyperbaric oxygenation (HBO) session and their combination on blood antistaphylococcal activity. Material and methods. Experiments were carried out on 77 outbred albino rats (females) exposed to LR (15—20% of the liver weight) and HBO at 3 ata as a 50-min session once daily, which was used in the operated rats in the first 3 days after LR. Serum bactericidal activity against opportunistic (No. 1726) and pathogenic (No. 209) S.aureus strains and the ability of neutrophils and monocytes to absorb S.aureus 209 were studied. Results. restoring the serum bactericidal activity against S.aureus 1726, HBO used after LR enhances its activity against pathogenic S.aureus 209. By decreasing the inhibitory effect of LR on the ability of the liver to enrich blood with the neutrophils that actively phagocy-tize the staphylococcus, HBO eliminates the retention of the monocytes actively phagocytizing S.aureus 209 in the operated organ, by concurrently increasing the count of these cells in the arterial blood. HBO stimulates the rate of uptake of S.aureus 209 by neutrophils in the operated organism when the blood passes through the vessels of the portal system with the partial retention of these cells in the liver portion left after its resection. By selectively suppressing the humoral component of blood antistaphylococcal defense, HBO in healthy unoperated animals stimulates the ability of the liver to enrich the blood with the monocytes that actively phagocytize the staphylococcus. At the same time the rate of uptake of S.aureus 209 by neutrophils is stimulated by hyperoxia. Conclusion. HBO regulates blood antistaphylococcal activity changes in response to LR by exerting a selective effect on the bactericidal activity of the blood against the staphylococcus in rats. Key words: liver, resection, hyperoxia, bactericidal activity, blood, staphylococcus.

Objective: to study body glutamine kinetics in hepatic failure and in the course use of hyperbaric oxygenation (HBO). Material and methods. Experiments were performed on 210 female albino rats. HBO was thrice conducted at 3 ata as a 50-min session once daily after hepatectomy (HE, 15—20% of the liver weight); glutamine levels were measured in their visceral organs and blood from the following vessels: the aorta, v. porta, v. hepatica, v. renalis. Results. By eliminating the glutamine-excretory dysfunction of the operated liver, HBO corrects its glutamine deficiency. At the same time, HBO activates glutamine production by gastrointestinal organs with its further incretion into the portal blood flow. It also stimulates the absorption of glutamine by lung tissue and its deamidation in the latter, but causes a reduction in myocardial glutamine concentrations. By stimulating the development of arterial hyperglutaminemia, HBO prevents the development of transient glutamine deficiency in the splenocytes and delayed postoperative portal hypoglutaminemia. HBO does not exert a substantial impact on brain tissue glutamine changes, but it regulates renal glutamine kinetic changes induced by partial HE. Conclusion. Hyperbaric oxygen used for hepatic failure induced by HE recovers body kinetic disorders of glutamine in this abnormality, by concurrently regulating the adaptive changes in its metabolism in the organs, which occur in response to liver damage. Key words: glutamine, metabolism, hepatic failure, hyperoxia.

Objective: to study ammonia kinetics in hepatic failure and in the course use of hyperbaric oxygenation (HBO) sessions. Material and methods. Experiments were carried out on 210 female albino rats. HBO was thrice conducted at 3 ata for 50 min once daily after hepatectomy (HE, 15—20% of the liver mass). Ammonium levels were determined in the visceral organs and blood from the following vessels: the aorta, v. porta, v. hepatica, v. renalis. Results. By preventing ammonia from entering the central bloodstream from the remaining postresection liver part and by restoring its ammonia-absorbing capacity, HBO creates conditions for eliminating arterial hyperammoniemia. HBO prolongs the inhibitory impact of HE on the entrance of ammonia from the gastrointestinal organs into the portal circulation, by preventing its selective accumulation in them, and decreases renal tissue ammonia concentrations. HBO keeps ammonia from being accumulated by cerebral cortical neurons, limits its lung accumulation, and creates conditions for its active neutralization by splenocytes in the posthy-peroxic period (PHP). At the same time HBO induces short-term activation of ammoniogenesis in thyroid and cardiac tissues, which should be considered as a sign of their enhanced functional activity. Conclusion. Hyperbaric oxygen eliminates ammonia kinetic disorders in the operated organism in HE-induced hepatic failure. The therapeutic effect of HBO remained by days 11 post-PHP. Key words: hyperoxia, ammonia, exchange, hepatic failure, organism, metabolism.

Objective: to define the role and place of hyperbaric oxygenation (HBO) in the treatment and prevention of liver cell failure. Material and methods. The results of the author’s own studies and the data available in the literature on the impact of HBO on the functional state of the liver and the whole organism in liver cell failure were analyzed. Results: The therapeutic and preventive effects of HBO during therapy for liver cell failure were due to the ability of hyperbaric oxygen to regulate metabolic processes in the sick organism. By eliminating the impaired hepatic neutralization of ammonia, hyperbaric oxygen corrects its extrahepatic reactions in rendering harmless various toxic substances, which become active in response to the ammonia-neutralizing dysfunction of hepatocytes. This prevents the development of endogenous ammonia intoxication. In liver cell failure, HBO concurrently stimulates hepatic protein synthesis function and the cell link of the body’s antimicrobial protection. The therapeutic effect of HBO is not always attended by the elimination of hepatic hypoxia and the sick organism’s hypoxemia, but it persists long in the posthyperoxic period. Conclusion: HBO can and must be an integral part of complex therapy for liver cell failure. Key words: hyperoxia, treatment, liver, failure.

Objective: to study the ability of hyperbaric oxygenation (HBO) to eliminate impaired phagocytosis-stimulating hepatic function caused by hepatectomy (HE). Material and methods. Experiments were conducted on 82 outbred female albino rats exposed to HE (15—20% of the organ mass) and HBO at 3 ata for 50 min once daily three times within the first three days after surgery. The capacities of neutrophils and monocytes of arterial (aorta) and venous (portal vein, hepatic veins) blood to ingest and digest S.aureus were investigated. Results: Under HBO, the inhibitory impact of HE on the phagocytosis-stimulating ability of the liver to S.aureus was limited for neutrophils and completely precluded for monocytes. In the posthyperoxic period, the phagocytosis-stimulating function of the operated liver was found to be active against the microbe being examined for both types of phagocytes. This was attended by inhibition of the anhepatic mechanisms responsible for the amplified phagocytic activity of neutrophils and monocytes, which were triggered in HE. HBO selectively regulated the arterial and venous blood content of neutrophils, by ingesting and digesting S.aureus as much as possible. HBO prevented the post-HE delay of the neutrophils and monocytes which actively englobed S.aureus in the operated organ. Conclusion: HBO eliminates HE-induced impairment of phagocytosis-stimulating function of the liver and creates conditions for its delayed activation by day 11 posthy-peroxia. Key words: hyperoxia, phagocytosis, regulation, liver, resection.