Prolonged exposure to hyperbaric oxygen induces neuronal damage in primaryrat cortical cultures

While seizure attack is one of the serious complications during the hyperba ric oxygen (HBO) therapy, there is still no direct evidence showing that HB O can induce neuronal damage in the brain. The objective of this study was first to investigate whether HBO would lead to neurotoxicity in the primary rat cortical culture. Second, since alterations in neurotransmitters have been suggested in the pathophysiology of central nervous system (CNS) oxyge n toxicity, the protective effects of the N-methyl-D-aspartate (NMDA) recep tor antagonism and nitric oxide (NO) synthase inhibition on the HBO-induced neuronal damage were examined. The results showed that HBO exposure to 6 a tmosphere absolute pressure (ATA) for 30, 60, and 90 min increased the lact ate dehydrogenase (LDH) activity in the culture medium in a time-dependent manner. Accordingly, the cell survival, measured by the 3,(4,5-dimethyl-2-t hiazolyl)2,5-diphenyl bromide (MTT) assay, was decreased after HBO exposure . Pretreatment with the NMDA antagonist MK-801 protected the cells against the HBO-induced damage. The protective effect was also noted in the cells p retreated with L-NG-nitroarginine methyl ester, an NO synthase inhibitor. T hus, our results suggest that activation of NMDA receptors and production o f NO play a role in the neurotoxicity produced by hyperbaric oxygen exposur e. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.