Effect of indomethacin on cerebral blood flow and development of oxygen convulsions.

Hyperbaric oxygenation modulates cerebral blood flow affecting the development of oxygen convulsions. Before hyperbaric oxygenation-induced convulsions in rats the initial decrease in blood flow gave place to hyperemia, Po(2) increased. In rats receiving cyclooxygenase inhibitor indomethacin no convulsions were observed, blood flow and Po(2)were lower than in controls. Our results indicate that indomethacin prevents hyperemia and alleviates oxygen convulsions under conditions of hyperbaric oxygenation.

Brain blood flow modulates the neurotoxic action of hyperbaric oxygen via neuronal and endothelial nitric oxide.

Studies on conscious rats with inhibition of NO synthase were used to assess the dynamics of brain blood flow and EEG traces during hyperbaric oxygenation at 4 or 5 atm. Oxygen at a pressure of 4 atm induced cerebral vasoconstriction in intact animals and decreased blood flow by 11-18% (p < 0.05) during 60-min exposure to hyperbaric oxygenation. Paroxysmal EEG activity and oxygen convulsions did not occur in rats at 4 atm of O2. At 5 atm, convulsive activity appeared on the EEG at 41 +/- 1.9 min, and blood flow decreased significantly during the first 20 min; blood flow increased by 23 +/- 9%, as compared with controls, (p < 0.01) before the appearance of convulsions on the EEG. Prior inhibition of NO synthase I (NOS I) and NO synthase III (NOS III) with N(omega)-nitro-L-arginine methyl ester (L-NAME, 30 mg/kg) or inhibition only of NOS I with 7-nitroindazole (7-NI, 50 mg/kg) prevented the development of hyperoxic hyperemia and paroxysmal spikes on the EEG during hyperbaric oxygenation at 5 atm. These results show that hyperbaric oxygen induces changes in cerebral blood flow which modulate its neurotoxic action via nitric oxide synthesized both in neurons and in cerebral vessels.

[Cerebral blood flow modulates hyperbaric oxygen induced neurotoxicity by neuronal and endothelial nitric oxide]. / Mozgovoi krovotok moduliruet neirotoksicheskoe deistvie giperbaricheskogo kisloroda s pomoshch'iu neironal'nogo i endotelial'nogo oksida azota.

The goal of work was to reveal changes in microcirculation of the rat brain and the role of nitric oxide (NO) in development of seizures at hyperbaric oxygen exposure. The Wistar rats with implanted paired platinum electrodes in left and right striatum were used for experiments. The latency of seizures was defined by the EEG, the cerebral blood flow (CBF) was measured by hydrogen clearance. One group of animals was exposed to a 5-ata oxygen, while the others before oxygen treatment were injected with: Nw-nitro-L-arginine methyl ester (L-NAME), blockator of constitutive NO synthase; 7-nitroindozol (7NI), specific inhibitor of neural NO synthase. The latency of seizures was 41 +/- 1.9 min at 5 ata oxygen exposure. CBF was decreased to 10-14% but before seizures it increased to 23 +/- 9%. L-NAME and 7NI prevented development of hyperoxygen hyperemia and onset of seizures. The results indicate occurrence of hyperbaric oxygen changes of the CBF that modulate neurotoxic effects of NO in neurons as well as in cerebral vessels.

[Cerebral blood flow dynamics in monkeys breathing a helium-oxygen mixture under high pressure]. / Dinamika mozgovogo krovotoka u obez'ian pri dykhanii geliokislorodnoi smes'iu pod vysokim davleniem.

Breathing with normoxic helium-oxygen mixture under high pressure successively induced tremor, myoclonia, seizures. Blood flow and the pO2 during the motor disorders increased, depending in the pressure, in the cortex, caudate nucleus, black substance and reticular formation.

The effect of increased nitrogen pressure on motor activity and the intercentral relationships of the brain of monkeys.

The influence of increased nitrogen pressure up to 19 ata was investigated in chronic experiments on monkeys of a species of Javan macaques (Macaca irus) with electrodes implanted in cortical and subcortical regions of the brain. The phasic character of the changes of motor activity of the animals, an increase in the spectral density of the average power of the EEG in the range of frequencies from 4 to 20 Hz, and a disturbance in the connectedness of the electrogenesis of the reticular formation of the midbrain with the bioelectrical processes in the substantia nigra, the head of the caudate nucleus, and the frontal and motoric areas of the cortex were identified in the course of nitrogen compression at a rate of 1.0 ata per 1 min.

[The superslow bioelectrical activity of the brain in monkeys during the development of the high-pressure nervous syndrome]. / Sverkhmedlennaia bioélektricheskaia aktivnost' mozga obez'ian pri razvitii nervnogo sindroma vyskogo davleniia.

In immersions over 20 ata, symptoms occur known as the high pressure neural syndrome (HPNS). Regular changes of the infraslow electrical activity were revealed in development of the HPNS: the waves of the 20-sec period start developing, the average oscillation amplitudes becoming considerably higher. The inter-lead correlation becomes more obvious.