腺苷A_1R在高压氧致中枢神经系统氧中毒发生中的作用研究

Effects of Adenosine A_1R in Central Nervous System Oxygen Toxicity Caused by Hyperbaric Oxygen Exposure

目的:探讨腺苷A1受体(A1R)在高压氧(hyperbaric oxygen,HBO)致中枢神经系统氧中毒(central nervous system oxygen toxicity,CNS-OT)发生中的作用。方法:(1)大鼠侧脑室注射A1R选择性激动剂CCPA后观察氧惊厥潜伏期。采用随机数字法将大鼠分为对照组和5μg、10μg以及20μg CCPA给药组。采用侧脑室注射方法分别给予生理盐水和不同剂量CCPA后,进行0.6MPa HBO暴露,记录大鼠的CNS-OT潜伏期。(2)大鼠侧脑室注射A1R选择性抑制剂DPCPX后观察氧惊厥潜伏期。采用随机数字法将大鼠分为对照组和15μg、30μg以及60μg DPCPX给药组。采用脑室注射方法分别给予DMSO和不同剂量DPCPX后,进行0.6 MPa HBO暴露,记录大鼠的CNS-OT潜伏期。结果:脑室注射5μg CCPA组(32.15分±0.8392分)、10μg CCPA组(60.50分±3.150分)和20μg CCPA组(70.91分±2.975分)惊厥潜伏期显著延长,差异有统计学意义(P<0.05)。脑室注射30μg DPCPX组(14.09分±1.363分)和60μg DPCPX组(8.564分±0.645分)惊厥潜伏期显著缩短,差异有统计学意义(P<0.05)。结论:中枢局部给予腺苷A1R选择性激动剂CCPA可以有效延长CNS-OT的潜伏期;中枢局部给予腺苷A1R选择性抑制剂DPCPX可以有效缩短CNS-OT的潜伏期。

Objective： To investigate the effects of adenosine A1 R in central nervous system oxygen toxicity（CNS-OT） caused by hyperbaric oxygen（HBO） exposure. Methods：（1） To observe the changes of CNS-OT latency when intracerebroventricularly injected with CCPA. 24 sprague-dawley rats were randomly divided into four groups. The rats in the control group were intracerebroventricularly injected with 20 μL saline, the rats in the 5 μg CCPA group were intracerebroventricularly injected with 5 μg CCPA, the rats in the 10μg CCPA group were intracerebroventricularly injected with 10 μg CCPA, and the rats in the 20 μg CCPA group were intracerebroventricularly injected with 20 μg CCPA. Then the latency of CNS-OT was observed and recorded on the exposure of 0.6MPa HBO.（2） To observe the changes of CNS-OT latency when intracerebroventricularly injected with DPCPX. 24 sprague-dawley rats were randomly divided into four groups. The rats in the control group were intracerebroventricularly injected with 20 μL DMSO, the rats in the 15 μg DPCPX group were intracerebroventricularly injected with 15 μg DPCPX, the rats in the 30 μg DPCPX group were intracerebroventricularly injected with 30 μg DPCPX, and the rats in the 60 μg DPCPX group were intracerebroventricularly injected with 60 μg DPCPX. Then the latency of CNS-OT was observed and recorded on the exposure of 0.6 MPa HBO. Results： The CNS-OT latency of 5 μg CCPA group was（32.15 min ±0.8392 min）, 10 μg CCPA group（60.50 min ±3.150 min） and 20 μg CCPA group（70.91 min ±2.975 min） were significantly longer than saline group（21.26 min ±0.9286 min）. The CNS-OT latency of 30 μg DPCPX group（14.09 min ±1.363 min） and 60 μg DPCPX group（8.564 min ±0.645 min） were significantly shorter than DMSO group（21 min±2.542 min）. Conclusion： The latency of central nervous system oxygen toxicity could be prolonged after intracerebroventricularly injecting adenosine A1 R agonist CCPA or shortened after intracerebroventricularly injecting adenosine A1 R antagonist DPCPX.