肌内皮缝隙连接对失血性休克大鼠血管收缩反应的影响  

Role of arterial myo-endothelial gap junction on the vascular contractile reactivity following hemorrhagic shock in rats

作　　者：明佳[1] 刘良明[1] 李涛[1] 杨光明[1] 徐竞[1] 

机构地区：[1]第三军医大学大坪医院野战外科研究所

出　　处：《中国危重病急救医学》2006年第9期519-522,共4页Chinese Critical Care Medicine

基　　金：国家重点基础研究发展计划"973"项目(2005CB522601)

摘　　要：目的研究肌内皮缝隙连接(MEGJ)对失血性休克大鼠内皮依赖性和非依赖性血管收缩反应的影响。方法56只SD大鼠按随机数字表法分为去甲肾上腺素(NE)组和杨梅黄酮组;NE组分为正常对照以及休克0、0.5、1和2h5个亚组;杨梅黄酮组分为正常对照以及休克0、0.5、1、2、3和4h7个亚组。各组取其肠系膜上动脉(SMA)制成血管环,分别测量在18α甘草次酸(18αGA)作用前后血管环对NE和杨梅黄酮反应性的变化。结果SMA血管环对NE的反应性表现为:休克0h和0.5h组明显高于正常对照组和其他休克时间点组,休克1h和2h组明显低于正常对照组和休克0h和0.5h组;18αGA对NE诱导的SMA血管环收缩反应性无明显影响。SMA血管环对杨梅黄酮的反应主要表现为:休克0、0.5、1和2h组明显高于正常对照组,于休克2h达最高点;休克3h和4h组明显低于正常对照组,运用18αGA阻断MEGJ后,各组血管环的收缩反应性较18αGA作用前明显下降,其中以休克1、2和3h组下降幅度明显大于其他组。结论失血性休克后早期,内皮依赖和非依赖性的血管收缩反应均有不同程度代偿性增加,休克1h和2h表现为非内皮依赖性血管收缩反应下降,休克3h和4h表现为内皮依赖性血管收缩反应明显降低;MEGJ在休克后内皮依赖性血管收缩反应的变化中起重要调节作用。Objective To observe the role of arterial myo-endothelial gap junction （MEGJ） on endothelium-dependent and independent vascular contractile reactivity following hemorrhagic shock in rats. Methods Fifty-six SD rats were randomly divided into noradrenaline （NE） group and myricetin group. NE group was further divided into 5 subgroups： normal control group, 0, 0. 5, 1 and 2 hours after hemorrhagic shock groups. Myricetin group was further divided into 7 subgroups： normal control group, 0, 0.5, 1, 2, 3 and 4 hours after hemorrhagic shock groups. Superior messenteric artery （SMA） was used to compare the changes in vascular responsing to NE or myricetin with or without 18α- glycyrrhetinic acid （18α- GA）. Results Compared with normal control group, the reactivity of SMA rings to NE was significantly increased at 0 and 0.5 hour after shock and then decreased at 1 hour and 2 hours after shock. 18a -GA had no effect on SMA constriction induced by NE. The reactivity of SMA rings to myricetin was increased at 0, 0.5, 1 hour and 2 hours after shock, and it reached the peak at 2 hours, then it significantly decreased at 3 hours and 4 hours after shock. 18α- GA antagonized SMA constriction induced by myricetin. The antagonizing effect on myricetin in shock 1, 2 and 3 hours groups was more obvious than that in the other groups. Conclusion At the early stage after hemorrhagic shock, the endothelium-dependent and independent vascular contractile response show a compensatory increase. The endothelium-independent contractile response is significantly decreased at 1 hour and 2 hours after shock, and the endothelium-dependent contractile response is significantly decreased at 3 hours and 4 hours after shock. MEGJ plays an important role in endothelium-dependent vascular contractile reactivity following hemorrhagic shock.

关 键 词：休克 失血性 内皮依赖性 血管收缩反应 肌内皮缝隙连接 

分 类 号：R459.7[医药卫生—急诊医学]