Abstract

Objective To investigate the role of adenosine in central nervous system oxygen toxicity induced by hyperbaric oxygen (HBO).Methods (1) Forty-eight mice were randomly divided into 2 groups:the control group (without any treatment) and the HBO group (exposed at 0.5 MPa HBO for 10 min).The contents of adenosine in the cortex were determined by using high performance liquid chromatography (HPLC).(2) Twenty-four Sprague-Dawley rats were randomly divided into 4 groups:the blank control group,the 40 μg adenosine treatment group,the 80 μg treatment group and 160 μg treatment group,each consisting of 6 animals.Animals in the above 4 groups were respectively given physiological saline and different levels of adenosine by injection into the cerebral cavity,then,they were exposed to HBO at a pressure of 0.6 MPa and latency of oxygen convulsion was recorded accordingly.Results HBO exposure could obviously elevate the level of adenosine in the cortex of mice.No statistical significance could be seen in latency of oxygen convulsion for the 40 μg adenosine treatment group[(22.71 ± 2.08)min] as compared with that of the control group [(21.25 ± 16.08)min] (P > 0.05).However,latencies of oxygen convulsion for the 80 μg adenosine treatment group[(35.40 ±6.08) min] and the 160 μg adenosine treatment group[(50.96 ± 12.10) min] were obviously prolonged,as compared with that of control group,with statistical significance(P < 0.05).And there existed a certain dose-effect relationship between them.Conclusions HBO exposure could elevate the level of adenosine in the cortex of the exposed animals.Local administration of adenosine in the cortex could effectively prolong the latency of central nervous system oxygen convulsion. Key words: Hyperbaric oxygen; Central nervous system oxygen toxicity; Adenosine

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