Oxygen Regime and Exchange of Ammonia in the Sensomotor Cortex of Cats During Blood Loss and Hyperbaric Oxygenation

Abstract

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.

Keywords

• hyperoxia
• blood loss
• brain
• oxygen
• ammonia
• metabolism