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Bidirectional influences of acetazolamide on central nervous system oxygen toxicity of rats.

Author(s): Huang JL, Zhang YL, Xiao X, Zhang JH, Lian QL, Liu Y, Sun XJ

Affiliation(s): Department of Nautical Medicine, Faculty of Naval Medicine, Second Military Medical University, Shanghai, PRC.

Publication date & source: 2010-09, Undersea Hyperb Med., 37(5):271-80.

Publication type: Research Support, Non-U.S. Gov't

Central nervous system oxygen toxicity, which occurs during diving and hyperbaric oxygen treatment, can lead to very dangerous situations, and it is of great importance to explore its mechanisms. We have speculated that cerebral blood flow plays a pivotal role in its occurrence. Except for acting as an anticonvulsant in clinical applications, acetazolamide is also a vasodilator used in both clinical and laboratory settings. In this study, when acetazolamide from 5 to 500 ug/kg body weight was administered by intracerebroventricular injection, the latency of central nervous system oxygen toxicity detected by electroencephalogram recording in rats subjected to hyperbaric oxygen at 6 atmospheres absolute was prolonged significantly. On the contrary, when the dose of intracerebroventricular injection achieved 5,000 ug/kg body weight, acetazolamide shortened the latency significantly. Intraperitoneal injection of acetazolamide more than 7.5 mg/kg body weight also shortened the latency significantly. Results also showed both intracerebroventricular injection of acetazolamide at a dose of 5,000 ug/kg body weight and intraperitoneal injection at dose of 7.5 mg/kg body weight inhibited the activity of carbonic anhydrase and increased the cerebral blood flow significantly, which helped aggravate oxidation damage and resulted in increased MDA and impaired glutathione peroxidase in brain tissue. But intracerebroventricular injection of acetazolamide at 5 ug/kg body weight had no effect on MDA and glutathione peroxidase, though it inhibited the activity of carbonic anhydrase. These observations indicated acetazolamide covers bidirectional influences on central nervous system oxygen toxicity. Within local brain tissue, especially neurons, it could exert its anticonvulsive effect on the central nervous system at low doses. On the other hand, under high doses, it would display its convulsive-hastening effect through increasing cerebral blood flow to aggravate the oxidation state of brain tissues and exacerbate central nervous system oxygen toxicity when subjected to hyperbaric oxygen. Blood flow of brain plays a pivotal role in central nervous system oxygen toxicity.

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