Effect of prostaglandin E2 and of indomethacin upon cerebral and pulmonary consequences of exposure to hyperbaric oxygen in rats

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Abstract
There is little data in the literature suggesting that endogenous prostaglandins (PG) might be involved in the pathomechanism of seizures. The mechanism of seizures inducted by exposure to O2 high pressure (OHP) is not fully elucidated the effect of exogenous PG and indomethacin (a PG synthesis inhibitor) on the development and consequences of seizures in rats exposed to OHP (5 ata, atm absolute pressure) was studied. In the animals pretreated with PGE2 (1 mg/kg s.c.) pre-seizure time was shortened, lung weight:body weight index increased and symptoms of respiratory failure potentiated as compared with the control group. Indomethacidn (5 mg/kg i.p.) prevented the development of seizures and of pulmonary consequences of OHP exposure. Biochemical examination of brains showed that the velocity of lipid free radical oxidation (reactions manifested by the breakdown of phospholipid fatty acids mainly unsaturated) was enhanced by OHP exposure and potentiated by pretreatment with PGE2. EM changes were similar to those seen in brain ischemia and/or hypoxia and the magnitude of changes was related to the intensity of symptoms evoked by OHP. Apparently cerebral and pulmonary consequences of OHP exposure are potentiated by exogenous PGE2 and prevented by inhibition of endogenous PG synthesis. PG and/or their active metabolites may be involved in the mechanism of O2 toxicity during exposure to hyperbaric O2.