Nitric oxide is involved in the mechanism of hyperbaric
oxygen (HBO(2)) brain toxicity as
nitric oxide synthase (NOS) inhibitors delay latent time before the onset of
seizures. The purpose of this study was to investigate if
seizures affect sensitivity to convulsions during subsequent exposure to HBO(2) and to determine if NOS activity and expression is changed after HBO(2)
seizures. Rats were exposed to 5 atm (gauge pressure) 100% O(2) until
seizures recorded by electroencephalograph (EEG) and reexposed 1, 2, or 6 days later. Latency to
seizures was significantly shorter (P<0.05) in animals reexposed 1 or 2 days after the first exposure. Activity of
calcium-dependent NOS activity in cortex was significantly higher 1 and 2 days after
seizures compared with controls (P<0.05), while
calcium-independent NOS activity was not changed during the 6-day post-seizure interval. The expression of neuronal NOS (nNOS)
protein determined by Western blot was higher 1 and 2 days after
seizures (P<0.05), while the expression of endothelial (eNOS) and inducible (iNOS) remained unchanged. nNOS upregulation 1 and 2 days after
seizures and protection against HBO(2)
seizures by nNOS-specific inhibitor
7-nitroindazole (7-NI) suggest possible involvement of NO in the mechanism of increased sensitivity to HBO(2) in reexposures.