Abstract
The effect of a previous exposure to hyperbaric oxygen (HBO) on the synthesis capacity of prostaglandin (PG) and thromboxane (TX) was investigated in the brain of male rats. Three groups of rats were used:
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1.
Neurotoxic HBO (n = 11): The rats were exposed to sixfold the atmospheric pressure (101.3 kPa), i.e., 6 absolute atmospheres (ATA), of pure O2 up to the first convulsion (6 ATA O2);
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2.
Mild hyperoxia (n = 10): The rats were exposed to compressed air at the same absolute pressure and for a similar time than that of the neurotoxic HBO group (here PO2 is 1.26 ATA);
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3.
Normoxia at atmospheric pressure (PO2 is 0.21 ATA) for control.
There was no convulsion in groups 2 and 3. Decompression of the high pressure groups lasted 15 min. After decapitation, samples of the frontal cortex and the striatum were taken, weighed, washed, and then incubated in Krebs-Ringer bicarbonate for 1 h. The release of eicosanoids in the medium was determined by enzyme immunoassay. Mild hyperoxia only significantly reduced in the striatum the release of 6-keto-PGF1α (1.3±2.4 vs 10.9±6.6 pg/mg wet tissue,p< 0.001; mean±SD) and PGE2 (3.2±2.7 vs 7.8±6.5 pg/mg wet tissue,p< 0.05), whereas TXB2 did not change. Neurotoxic hyperoxia reduced significantly in both cortex and striatum the release of 6-keto-PGF1α (8.7±5.1 vs 29.3±13.0,p< 0.001 and 3.2±4.3 vs 10.9±6.6,p< 0.01 respectively) and PGE2 (8.3± 5.8 vs 15.2± 6.4,p < 0.05 and 3.1± 2.9 vs 7.8±6.5,p< 0.05 respectively) without affecting TXB2 release. These inactivations could be related to reactive oxygen species (ROS) induced by HBO. Taking into account the known sensitivities to ROS of the enzymes of the eicosanoid cascade, the effects of HBO on PGs could be related to a hyperoxic deactivation of PGI synthase in striatum, beginning with nonneurotoxic hyperoxia with a possible associated deactivation of PGE synthase activity in both cortex and striatum in hyperbaric neurotoxic hyperoxia. The decrease in 6-keto-PGF1α reflecting the decrease in prostacyclin could lead to vasoconstriction (which in turn decreased local oxygen partial pressure) and also to platelet aggregation, since TXB2 was not affected in the process. As this inactivation began well before the neurotoxicity threshold of HBO, the following changes in eicosanoids may therefore take some non-specific part in the HBO-induced brain damage.
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References
Balentine J. D. (1982)Pathology of Oxygen Toxicity. Academic, New York.
Bazan N. G. (1970) Effects of ischemia and electroconvulsive shock on free fatty acid pool in the brain.Biochim. Biophys. Acta 218, 1–10.
Bennett P. B. (1982) Inert gas narcosis, inThe Physiology and Medicine of Diving (Bennett P. B. and Elliott D. H., eds.), pp. 239–261, Best, San Pedro, CA.
Bertharion G. and Barthélémy L. (1964) Effet aigu de 1’ oxygéne hyperbare.Agressologie 5, 583–593.
Brannan T. S., Maker H. S., Weiss C., and Cohen G. (1980) Regional distribution of glutathione peroxidase in the adult rat brain.J. Neurochem. 35, 1013,1014.
Clark J. M. (1974) The toxicity of oxygen.Am. Rev. Resp. Dis. 110, 40–50.
Dubois A., Danquechin Dorval E., Steel L., Fiala N. P., and Conklin J. J. (1987) Effect of ionizing radiation on prostaglandins and gastric secretion in rhesus monkeys.Radiat. Res. 110, 289–293.
Föstermann U., Heldt R., and Hertting G. (1983) Increase in brain prostaglandins during convulsions is due to increased neuronal activity and not to hypoxia.Arch. Int. Pharmacodyn. 263, 180–188.
Francois C., N’Guyen-Legros J., and Percheron G. (1981) Topographical and cytological localisation of iron in rat and monkey brains.Brain Res. 215, 317–322.
Freeman, B. A. and Crapo J. D. (1982) Free radicals and tissue injury.Lab. Invest. 47, 412–426.
Gerschman R., Gilbert D. L., Nye S. W., Dwyer P., and Fenn W. O. (1954) Oxygen poisoning and X-irradiation: a mechanism is common.Science 119, 623–626.
Jacobs T. P., Shohami E., Baze W., Burgard E., Gunderson C., Hallenbeck J. M., and Feuerstein G. (1987) Deteriorating stroke model: histopathology, edema and eicosanoid changes following spinal cord ischemia in rabbits.Stroke 18, 741–750.
Jenkinson S. G., Jordan J. M., and Lawrence R. A. (1988) BCNU-induced protection from hyperbaric hyperoxia: role of glutathione metabolism.J. Appl. Physiol. 65, 2531–2536.
Mayevsky A. (1984) Brain oxygen toxicity, inUnderwater Physiologie VIII (Barach A. J. and Matzen M. M., eds.), pp. 69–89, Undersea Medical Society, Bethesda, MD.
Mialon P. and Barthélémy L. (1991) The influence of one hyperbaric oxygeninduced seizure on brain eicosanoid content.Mol. Chem. Neuropathol. 15, 1–11.
Mialon P., Caroff J., Barthélémy L., and Bigot J. C. (1990) Ammonia and monoamines concentrations in two brain areas in rats after one hyperoxic seizure.Aviat. Space Environ. Med. 61, 28–32.
Mialon P., Gibey R., Bigot J. C., and Barthélémy L. (1992) Changes in striatal and cortical amino acid and ammonia levels of rat brain after one hyperbaric oxygen-induced seizure.Aviat. Space Environn. Med. 63, 287–291.
Moncada S. and Vane J. R. (1979) Pharmacology and endogenous roles of prostaglandin endoperoxides, thromboxane A2 and prostacyclin.Pharmacol Rev. 30, 293–320.
Noda Y., McGeer P. L., and McGeer E.G. (1983) Lipid peroxide distribution in brain and the effect of hyperbaric oxygen.J. Neurochem. 40, 1329–1332.
Novick W. I. (1966) Effect of oxygen tension on monoaminase activity.Biochem. Pharmacol. 15, 1009–1012.
Piantadosi C. A. and Tatro L. G. (1990) Regional H2O2 concentration in rat brain after hyperoxic convulsions.J. Appl. Physiol. 69, 1761–1l766.
Pradelles P., Grassi J., and Maclouf J. (1985) Enzyme immunoassays of eicosanoids using acetylcholine esterase as label: an alternative to radioimmunoassay.Anal. Chem. 57, 1170–1173.
Ruszczewski P., Truskolaski P., Dabrowiecki Z., Rap Z. M., and HerbaczynskaCedro K. (1979) Effect of prostaglandin E2 and of indomethacin upon cerebral and pulmonary consequences of exposure to hyperbaric oxygen in rats.Acta Neurol. Scand. 59, 188–199.
Setty B. N. Y., Walenga R. W., and Stuart M. J. (1984) Kinetic analyses of the effect of hyperoxia and hypoxia on vascular cyclooxygenase activity in vitro.Biochem. Biophys. Res. Commun. 125, 170–176.
Shimizu T. and Wolfe L. (1990) Arachidonic acid cascade and signal transduction.J. Neurochem. 55, 1–13.
Shohami E. and Gross J. (1985) An ex vivo method for evaluating prostaglandin synthetase activity in cortical slices of mouse brain.J. Neurochem. 45, 132–136.
Shohami E., Rosenthal J., and Lavy S. (1982) The effect of incomplete cerebral ischemia on prostaglandin levels in rat brain.Stroke 13, 494–498.
Smith L. J., Sommers E., Hunt C. E., and Pachman L. (1986) Hyperoxic lung injury in mice: a possible protective role for prostacyclin.J. Lab. Clin. Med. 108, 479–488.
Torbati D., Parolla D., and Lavy S. (1976) Changes in the electrical activity and PO2 of the rat’s brain under high pressure oxygen.Exp. Neurol. 50, 439–447.
Weidenfeld J., Lysy J., and Shohami E. (1987) Effect of dexamethasone on prostaglandin synthesis in various areas of the rat brain.J. Neurochem. 48, 1351–1354.
Whorton A. R., Mongomery M. E., and Kent R. S. (1985) Effect of hydrogen peroxide on prostaglandin production and cellular integrity in cultured procine aortic endothelial cells.J. Clin. Invest. 76, 295–302.
Wolfe L. S. and Coceani F. (1979) The role of prostaglandins in the central nervous system.Ann. Rev. Physiol. 41, 669–684.
Yusa T., Crapo J. D., and Freeman B. A. (1984) Liposome-mediated augmentation of brain SOD and catalase inhibits CNS O2 toxicity.J. Appl. Physiol.: Respir. Environ. Physiol. 57, 1674–1681.
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Mialon, P., Barthélémy, L. Effect of hyperbaric oxygen on prostaglandin and thromboxane synthesis in the cortex and the striatum of rat brain. Molecular and Chemical Neuropathology 20, 181–189 (1993). https://doi.org/10.1007/BF02815371
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DOI: https://doi.org/10.1007/BF02815371