Effects of dilating cerebral arierioles by actetazolamide on central nervous system oxygen toxicity

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Author:
HUANG Jun-long(Department of Nautical Medicine,Faculty of Naval Medicine,the Second Military Medical University,Shanghai 200433,China)
XIAO Xiang(Department of Nautical Medicine,Faculty of Naval Medicine,the Second Military Medical University,Shanghai 200433,China)
LIU Yun(Department of Nautical Medicine,Faculty of Naval Medicine,the Second Military Medical University,Shanghai 200433,China)
JIANG Chun-lei(Department of Nautical Medicine,Faculty of Naval Medicine,the Second Military Medical University,Shanghai 200433,China)
Journal Title:
CHINESE JOURNAL OF NAUTICAL MEDICINE AND HYPERBARIC MEDICINE
Issue:
Volume 15, Issue 06, 2008
DOI:
Key Word:
Hyperbaric oxygen; Oxygen toxicity; Seizure; Cerebral blood flow; Acetazolamide

Abstract´╝Ü Objective To investigate effects of dilating ceretral arteriolesty acetazolamide on central nervous system oxygen toxicity (CNS-OT). Methods In this study, latency to CNS-OT of rats with intraperitoneal injection of acetazolaimide, was determined and then cerebral blood flow and content of maleic dialdehyde (MDA) was measured, and also glutamic acid decarboxylase (GAD) was tested. Results CNS-OT latency of rats which were injected with acetazolamide intraperitoneally was shortened significantly ( P < 0. 05 , P <0. 01). Acetazolamide could dilate the brain arterioles to increase the cerebral blood flow remarkably (P<0. 01 ). The content of MDA of different brain area in groups treated with intraperitoneal injection of acetazolamide increased significantly (P <0. 05). And leuel of GAD in group treated with acetazolamide was reduced remarkably (P < 0. 01 ). Conclusions Acetazolamide shortened the latency to CNS-OT probably through its dilating cerebral arterioles to aggravate the oxidative damage and reduced content of GAD in brain. It could promote the incidence of acute oxygen poisoning.

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