The purpose of the present study was to explore the relation between the modulation of cerebral blood flow and the latency of hyperbaric
oxygen-induced convulsion. There were two parts in this study. First, the effect of
acetazolamide or (and)
indomethacin on the latency of hyperbaric
oxygen-induced convulsion was observed. Seventy Sprague-Dawley (SD) rats were randomly divided into 7 groups: the
acetazolamide 200, 20, 10, 7.5, 5, 2.5 mg/kg
body weight and
normal saline (NS) group. Forty rats were divided into 5 groups:
indomethacin 20, 10, 5, 2.5 mg/kg
body weight and NS groups. Another 40 rats were divided into 5 groups which were administered with
indomethacin in the dose of 0 mg/kg (NS), 0 mg/kg (
NS), 5, 10 and 20 mg/kg
body weight. Thirty min later the first group was given NS, and all the other four groups were given
acetazolamide with a dose of 7.5 mg/kg
body weight. The animals were given
acetazolamide or (and)
indomethacin intraperitoneally, and 20 min later they were exposed to the pressure of 6 ATA (absolute atmosphere) of pure
oxygen. The time from exposure to the onset of
seizure (clonic-tonic convulsion) was recorded for each animal according to behavioral observation. Second, the change of
maleic dialdehyde (MDA) was measured after
acetazolamide and (or)
indomethacin treatment. Seventy-two SD rats were randomly divided into 9 groups: Control, 6 and 16 min respectively with NS,
acetazolamide,
indomethacin, and both
acetazolamide and
indomethacin group. The dose of
acetazolamide was 7.5 mg/kg
body weight and the dose of
indomethacin was 20 mg/kg
body weight. After injection of drugs, the animals were subjected to the pressure of 6 ATA of pure
oxygen in respect to its time course group. Then the rats were decapitated and the cerebral cortex was dissected and homogenized. The content of MDA was determined. We found that (1) when the dose of
acetazolamide is higher than 7.5 mg/kg, it shortened the latency to hyperbaric
oxygen-induced convulsion significantly (P<0.05, P<0.01). There was no significant difference in the latency between every to hyperbaric
oxygen-induced convulsion significantly (P<0.05, P<0.01). There was no significant difference in the latency between every two groups of rats treated with different doses of
indomethacin. But when the rats were administered
acetazolamide of 7.5 mg/kg
body weight after being pretreated with
indomethacin of 20 mg/kg
body weight, the outbreak of convulsion was put off remarkably (P<0.05). (2) In comparison with the control, the content of MDA in the group treated with
acetazolamide increased significantly (P<0.01), but when the rats were treated with both
acetazolamide and
indomethacin, the content of MDA was reduced significantly both in 6 and 16 min exposure time projects (P<0.05, P<0.01). These results suggest that
acetazolamide which dilates the brain arterioles can obviously shorten the latency of hyperbaric
oxygen-induced convulsion and aggravate the oxidation of the brain.
Indomethacin can resist acetazolamideos effect on the latency and oxidation level when the animals were exposed to the hyperbaric
oxygen. The activity of
carbonic anhydrase correlates closely with the oxidation injury.