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The purpose. To study the effect of partial hepatectomy (PH) on the main ways of ammonia detoxication in the liver (synthesis of urea and glutamine) in chronic tetrachlorcarbon (CCl4) hepatitis. Methods. The experiments were performed on 165 white outbred rats (females) weighing 180-220 g Chronic CCl4-hepatitis was reproduced by subcutaneous injection of 50% CCl4 solution in olive oil (0.1 ml/100g of body weight,65 days, through the day with two two-week breaks between 6-7 and 13-14 injections). PH conducted electrocautery, removing part of the left lobe of the liver (15-20% by weight of the body) to 65th (and last) day of the introduction of the CCl4. Animals were studied after 65 days of development of CCl4-hepatitis on day 3, 7 and 14 days after laparotomy («falsely operated» animals) and partial hepatectomy. In subcellular fractions of the liver investigated the activity of phosphatdependent glutaminase (FDG), glutamatdehydrogenaze (GDG), glutaminsintetaze (GS), arginase. In the liver tissue investigated the content of ammonia, glutamine, glutamate and urea. Results. Found that on 65-th day of the development of CCl4 in the liver decreases the concentration of ammonia, glutamine, glutamate, urea, and activity of GS, GDG and arginase. Activity FDG was not changed. The use of PH on the background of chronic CCl4-hepatitis has a short-term (3 days) a stimulating effect on the activity FDG, GS, postponed (14 days) the inhibitory effect on the activity of GDG. This was accompanied by an increase in the concentration in the liver of ammonia within 14 days of the postoperative period on the background of maintaining reduced concentrations of glutamine and glutamate it. The stimulatory effect of CHA on the activity of arginase is saved to the 14th day of the postoperative period, however, the concentration of urea in the liver remained below normal. Conclusions. The obtained results show that CGA on the background of chronic hepatitis increases the pathological impact of CCl4 on amniocentesis liver function.

Activity of phosphate-dependent glutaminase was determined in hepatocytes of white female rats, both in healthy animals and in rats with chronic CCl4-hepatitis on day 3 after liver resection and hyperbaric oxygenation. In healthy animals, activity of phosphate-dependent glutaminase was not altered after hepatic resection, but it was elevated in animals with chronic CCl4-hepatitis. Hyperbaric oxygenation inhibited activity of hepatocytic phosphate-dependent glutaminase in non-operated healthy rats but stimulated it after hepatic resection. In animals with chronic CCl4-hepatitis; hyperbaric oxygenation restricted the stimulating effect of hepatic resection on phosphate-dependent glutaminase activity.

Application of hyperbaric oxygenation (HBO, 3 ata, 1 session for 50 min per day) during the first three days after liver resection (LR, 15-20% from the organ mass) in animals with chronic toxic hepatitis (CCl4, 50%, 0,1 ml/per 100 g of body mass, subcutaneously, once in 2 days, 65 days) eliminates a deficit of glutamine and glutamate in an operated liver and prevents accumulation of the endogenic toxin, ammonia, caused by combined effects of CCl4 and LR. Thus hyperbaric oxygen modulates the effect of the LR on the activity of key enzymes of the glutamine metabolism in liver: glutamine synthetases (GS) and phosphate-dependent glutaminases (PDG). HBO enhanced and prolonged the LR effect of the GS activity and restricted analogous changes in PDG during an early (3 day) postoperative period and promoted a delayed transient stimulation in the late (7 day) postoperative period. In contrast to non-oxygenated animals with LR this was not accompanied by accumulation of ammonia and the decrease in glutamine concentration in the liver.

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.

The study was undertaken to examine nitrogen metabolism in gastrointenstinal tract tissues in endogenous ammonia intoxication caused by liver resection (LR) and the impact of three-day hyperbaric oxygenation (HBO) on the metabolism. The albino rat samples of arterial (aortic) and venous (portal) blood and the tissues of the stomach, duodenum, and large bowel were the subject of this investigation. HBO was made thrice at 3 ata as a 50-min session within the first three days after LR (15-20% of the mass of the organ). The levels of ammonia, glutamine, and urea were measured. HBO prevents postoperative arterial hyperammonemia, the gastrointestinal accumulation of ammonia, by reducing its accumulation in the portal blood. HBO stimulates the development of LR-caused portal hyperglutaminemia and the decrease of GIT tissue uptake of "arterial" glutamine and regulates the influence of an operation on the levels of this metabolite in GIT tissues. HBO elevates the content of urea in the arterial and portal blood, without affecting the LR-induced change in its GIT tissue concentration. Hyperbaric oxygen regulates adaptive GIT tissue nitrogen metabolic reactions caused in response to liver resection.

Employment of hyperbaric oxygenation (HBO, 3 bar, 50 min, 1 session per day) during the first three days after resection of liver (15-20% of mass) normalized glutamine metabolism impairments caused by operational trauma.

The experimental study has established that a 15-20% resection of a hepatic mass in healthy rats inhibits glutamine formation in hepatocytes and stimulates its decomposition in liver cells promoting ammonia accumulation in the operated liver. The hepatocyte urea synthetizing cycle can not prevent accumulation of ammonia in the liver and raise their urea content even if arginase activity is high. Inhibition of GDG activity in the operated liver not only limits formation of ammonia during glutamate deamination but also results in glutamine deamination inhibition in hepatocytes. These disorders of hepatocytic ammonia neutralizing function persist for 21 days after hepatic resection.

A long-term treatment of female rats with CCl4 caused a decrease of glutamine content in the liver. This decrease may be attributed to stable reduction of glutamine synthetase activity and slightly elevated (or unchanged) phosphate-dependent glutaminase. Partial hepatectony (15-20% of the liver) did not normalise glutamine metabolism.

The experiments have shown that even resection of relatively small (15-20%) portion of the intact liver resulted in significant changes of glutamine metabolism in hepatocytes, which were not eliminated for 21 days of postoperative period. The changes of the activity of key enzymes of glutamine metabolism, glutamine synthetase and glutaminase (phosphate-dependent), are responsible for these alterations. The changes of activity of these enzymes closely depend on the location of hepatocytes to focus of mechanical damage.

The status of the main routes of ammonium detoxication in the liver (synthesis of glutamine and urea) after its resection and hyperbaric oxygenation (HBO) was studied in 160 rats. HBO (3 sessions at 3 atm. abs.--50 min) following resection of the liver stimulated the activity of glutamine synthase and prevented the reduction of glutamate (a substrate for glutamine synthesis) level in the operated on liver. Hyperbaric oxygen activated the glutamine-dependent and non-glutamine-dependent pathways of urea synthesis in the resected liver and ensured the incorporation of glutamine amido groups in the ornithine cycle. HBO boosted the inhibitory effect of liver resection on the activity of glutamate dehydrogenase and prevented the accumulation of ammonium in the hepatocytes of resected liver. The stimulating effect of HBO on the ammonium-detoxifying function of the resected liver persisted for 11 days after the exposure.

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.