1. Prolonged exposure to hyperbaric oxygen induces neuronal damage in primary rat cortical cultures.
- Author
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Huang KL, Wu JN, Lin HC, Mao SP, Kang B, and Wan FJ
- Subjects
- Animals, Cell Survival drug effects, Cells, Cultured, Cerebral Cortex metabolism, Cerebral Cortex pathology, Culture Media, Conditioned metabolism, Dizocilpine Maleate pharmacology, Enzyme Inhibitors pharmacology, Excitatory Amino Acid Antagonists pharmacology, L-Lactate Dehydrogenase metabolism, NG-Nitroarginine Methyl Ester pharmacology, Neurons metabolism, Neurons pathology, Neuroprotective Agents pharmacology, Nitric Oxide Synthase antagonists & inhibitors, Nitric Oxide Synthase Type I, Pressure, Rats, Rats, Sprague-Dawley, Receptors, N-Methyl-D-Aspartate antagonists & inhibitors, Tetrazolium Salts, Thiazoles, Cerebral Cortex drug effects, Hyperbaric Oxygenation adverse effects, Neurons drug effects, Oxygen toxicity
- Abstract
While seizure attack is one of the serious complications during the hyperbaric oxygen (HBO) therapy, there is still no direct evidence showing that HBO 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) oxygen toxicity, the protective effects of the N-methyl-D-aspartate (NMDA) receptor antagonism and nitric oxide (NO) synthase inhibition on the HBO-induced neuronal damage were examined. The results showed that HBO exposure to 6 atmosphere absolute pressure (ATA) for 30, 60, and 90 min increased the lactate dehydrogenase (LDH) activity in the culture medium in a time-dependent manner. Accordingly, the cell survival, measured by the 3,(4,5-dimethyl-2-thiazolyl)2, 5-diphenyl-tetrazolium 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 pretreated with L-N(G)-nitro-arginine methyl ester, an NO synthase inhibitor. Thus, our results suggest that activation of NMDA receptors and production of NO play a role in the neurotoxicity produced by hyperbaric oxygen exposure.
- Published
- 2000
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