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Publication AbstractsIntrasynaptosomal free calcium and nitric oxide metabolism in central nervous system oxygen toxicityWang WJ, Ho XP, Yan YL, Yan TH, Li ClAviat Space Environ Med 1998; 69:551-5 AbstractBackground: Central nervous system (CNS) oxygen (O2) toxicity is complex, and the etiology of its most severe manifestation, O2 convulsions, is yet to be determined. A role for nitric oxide (NO) has been proposed, although recent data have indicated that NO is synthesized from L-arginine by an enzyme, NO synthase (NOS). The enzyme is dependent on free calcium (Ca2+) concentration, therefore increases in intracellular Ca2+ may constitute the physiological and pathophysiological mechanisms for stimulating the snythesis of NO. Methods: In this study, the intrasynaptosomal free calcium concentration ([Ca2+]) was measured by the fluorescence of fura-2/AM, and cGMP (as an indirect marker of NO levels) was by radioimmunoassay (RIA) in the rat hippo-campus after hyperbaric oxygen (HBO) exposure. We also investigated the effects of daurisoline (DSL, calcium channel blocker) and N- nitro-L-arginine (LNNA, NOS inhibitor) on the above biochemical parameters and the development of oxygen toxicity. Results: The results show that when the rats were exposed to HBO at 0.5 Mpa the intrasynaptosomal Ca2+ and cGMP levels increased by two and three times, respectively, whereas with the use of DSL prior to HBO, the accumulation of [Ca2+]i and cGMP dropped to 56% and 60%, correspondingly. In the rats medicated with LNNA prior to HBO, [Ca2+]i and cGMP levels dropped to 70% and 36% of the HBO group. At the same time, the appearance of CNS oxygen toxicity was delayed and the survival rate increased. The protective effects of LNNA were reversed by L-arginine pretreatment. These findings suggest that the neuronal Ca2+ overload during HBO exposure is a major factor in the pathogenesis of CNS O2 toxicity, and cGMP-NO pathways may be directly involved in HBO-induced seizures.
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