| 陈宇亮 张亚楠 李靖 张婷 李润平.腺苷A1R在高压氧致中枢神经系统氧中毒发生中的作用研究[J].,2015,15(17):3216-3219 |
| 腺苷A1R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 A1R in Central Nervous SystemOxygen ToxicityCaused by Hyperbaric Oxygen Exposure |
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| DOI： |
| 中文关键词: 高压氧 中枢神经系统氧中毒 腺苷A1受体 |
| 英文关键词: Hyperbaric oxygen Central nervous systemoxygen toxicity Adenosine A1R |
| 基金项目:国家自然科学基金项目（81272179）；第二军医大学军事医学专项课题（2011JS02） |
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| 中文摘要: |
| 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5 ug、10 ug以及20 ug 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0.6
MPa 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15 滋g、30 滋g 以及60 滋g 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5 ug CCPA 组（32.15 分± 0.8392 分）、10 ug CCPA 组
（60.50 分± 3.150 分）和20 滋g 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30 ug
DPCPX 组（14.09 分± 1.363 分）和60 ug 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。 |
| 英文摘要: |
| Objective:To investigate the effects of adenosine A1R 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 uL saline, the rats in the 5 滋g CCPA group were intracerebroventricularly injected with 5 ug CCPA, the rats in the 10
ug CCPA group were intracerebroventricularly injected with 10 ug CCPA, and the rats in the 20 ug CCPA group were
intracerebroventricularly injected with 20 ug CCPA. Then the latency of CNS-OT was observed and recorded on the exposure of 0.6
MPa 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 uL DMSO, the rats
in the 15 ug DPCPX group were intracerebroventricularly injected with 15 ug DPCPX, the rats in the 30 ug DPCPX group were
intracerebroventricularly injected with 30 ug DPCPX, and the rats in the 60 ug DPCPX group were intracerebroventricularly injected
with 60 ug 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 ug CCPA group was (32.15 min ± 0.8392 min), 10 ug CCPA group (60.50 min ± 3.150 min) and 20 ug 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 ug DPCPX
group (14.09 min ± 1.363 min) and 60 ug 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 A1R agonist CCPA or shortened after intracerebroventricularly injecting adenosine A1R antagonist DPCPX. |
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