肌内皮缝隙连接对失血性休克大鼠血管收缩反应的影响

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（18α-GA）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；18α-GA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18α-GA阻断MEGJ后，各组血管环的收缩反应性较18α-GA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。

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

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 18alpha-glycyrrhetinic acid (18alpha-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. 18alpha-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. 18alpha-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.