Na＋／K＋泵参与缺氧诱发的大鼠脑血管收缩的体外研究  

Na^+,K^+-ATPase involes in contraction of rat cerebral artery induced by anoxia

作　　者：孟岩[1] 罗红[2] 任晓华[1] 王永利[2] 

机构地区：[1]石家庄市中心医院临床药学室,河北石家庄050011 [2]河北医科大学河北省新药药理毒理重点实验室,河北石家庄050017

出　　处：《中国药理学通报》2013年第9期1307-1312,共6页Chinese Pharmacological Bulletin

基　　金：河北省自然科学基金项目(No 301360)

摘　　要：目的探讨Na+/K+泵是否参与缺氧诱发的脑血管收缩。方法以PSS、K-PSS、oua-PSS、oua-K-PSS或K-free-PSS液灌流大鼠离体基底动脉后5、10、15、30和60 min时,以压力肌动描记系统记录缺氧前后血管直径的变化。结果缺氧、K+和哇巴因灌流均可使大鼠基底动脉产生明显收缩,缺氧可增强K+、10-8和10-7mol·L-1哇巴因对正常基底动脉的收缩(P<0.01),但对K+与10-8或10-7mol·L-1哇巴因共同预收缩的基底动脉以及5×10-7mol·L-1哇巴因收缩的基底动脉并无影响。而且用可取消Na+/K+泵活性的无K+-PSS液,不管在正常或缺氧情况下,均能使基底动脉在5min内达到最大收缩。结论 Na+/K+泵可能参与了缺氧诱发的脑血管收缩,其机制可能与缺氧抑制Na+/K+泵有关。Aim To explore whether Na ＋ , K ＋ -ATPase involves in the effect of anoxia on the vasoconstriction. Methods The isolated basilar artery was perfused with PSS, K-PSS, oua-PSS, oua-K ＋ -PSS, or K＋ -free- PSS under normal or anoxia condition and the diameter changes were recorded by Pressure Myogragh System （Model 120CP, Danish Myo Technology A/S） in 5, 10, 15, 30 and 60 .rain after perfusion. Results All of anoxia, ouabain and high K＋ induced significant contraction of isolated rat basilar arteries. Anoxia could enhance the contraction of rat basilar arteries preincu- bated by K＋ , 10-8 and 10-7 mol · L-1 ouabain, but did not affect the contraction of isolated rat basilar ar-tery induced by co-incubation of K＋ plus 10-s or 10 -7 mol · L-1 ouabain and induced by 5 × 10-7 tool · L ^-1 ouabain. And K-free-PSS, which abolishes the activity of Na ＋ , K ＋ -ATPase, generated the maximal contrac- tion of rat basilar arteries within 5 rain, either in nor- mal or anoxic condition. Conclusion Anoxia results in the contraction of cerebral vessels. Na＋, K ＋-AT- Pase involves in anoxic contraction of cerebral vessels. Its mechanism may relate to the activity of the Na ＋ , K ＋ -ATPase lowered by anoxia.

关 键 词：Na＋ K＋泵 缺氧 哇巴因 基底动脉 血管收缩 大鼠 

分 类 号：R-332[医药卫生] R322.81