[Effect of acetazolamide on the latency of hyperbaric oxygen-induced convulsion].

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 on the latency of hyperbaric oxygen-induced convulsion was observed. 32 Sprague-Dawley (SD) rats were randomly divided into four groups: the acetazolamide 200, 20, 2 mg/kg body weight and normal saline (NS) group. The animals were given intraperitoneally acetazolamide or NS, respectively, before being 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 changes in maleic dialdehyde (MDA) and the activity of glutathione peroxidase (GSH-PX) were measured after acetazolamide treatment. 40 SD rats were randomly divided into five groups: NS group, 6 min with NS group, 6 min with acetazolamide group, 16 min with NS group, and 16 min with acetazolamide group. The dose of acetazolamide was 20 mg/kg body weight. After injection of NS or acetazolamide, the animals were subjected to the pressure of 6 ATA of pure oxygen in respect to its time course group. The rats were decapitated and the cortex, hippocampus, and striatum of brains were dissected and homogenized. The content of MDA and the activity of GSH-PX in these tissues were determined. We found that (1) there was a significant difference in the latency of hyperbaric oxygen-induced convulsion between the acetazolamide 200 mg/kg group and the NS control group, as well as between the acetazolamide 20 mg/kg group and the NS control group (P<0.01), whereas there was no significant difference between the NS group and the acetazolamide 2 mg/kg weight group (P>0.05). The latency of these groups were listed as follows: 9.78+/-1.94 min for 200 mg/kg body weight group, 10.92+/-1.68 min for 20 mg/kg body weight group, 24.32+/-4.33 min for 2 mg/kg body weight group and 22.02+/-4.32 min for NS control group. (2) there was no significant difference between all groups in the activity of GSH-PX, though it varied with the oxidation levels. In the cortex and hippocampus, the activity of GSH-PX boosted up at first, but with the progress of the oxidation it was impaired. In the striatum, the activity of GSH-PX increased stepwise with the aggravation of the oxidation. The MDA content in the cortex increased significantly in the group of 6 min with acetazolamide (P<0.01), as well as the group of 16 min with acetazolamide group both in cortex and hippocampus (P<0.01, P<0.05). The MDA content of all groups is correlated with the dose of acetazolamide and the exposure time. These results suggest that acetazolamide which dilates the brain arteriolar obviously shortens the latency of hyperbaric oxygen-induced convulsion, and that acetazolamide dilates the vessels and increases the supply of the oxygen breaking into the brain tissues and aggravates the oxidation. The hyperbaric oxygen-induced convulsion correlates closely with the oxidation injury.