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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.