肌内皮缝隙连接在失血性休克大鼠内皮依赖和非内皮依赖的血管舒/缩功能调节中的作用

    Effects of Myo-Endothelial Gap Junction on the Endothelium-Dependent and -Independent Vascular Relaxation/Constriction in Hemorrhagic Shock Rats

    • 摘要: 目的 研究肌内皮缝隙连接(myo-endothelial gap junction,MEGJ)通道在失血性休克大鼠肠系膜上动脉血管(SMA)的内皮依赖和非内皮依赖的血管收缩/舒张功能调节中的作用。方法 利用在体血管管径测定技术,观察MEGJ的阻断剂18α-甘草次酸(18α-GA)对非内皮依赖的血管收缩剂去甲肾上腺素(NE)和舒张剂硝普钠(SNP)、以及对内皮依赖的血管收缩剂杨梅黄酮和舒张剂乙酰胆碱(ACh)诱导的休克大鼠血管舒/缩功能的影响。结果 18α-GA(2 mg·kg-1)对非内皮依赖的血管舒张剂SNP(10 μg·kg-1)诱导的失血性休克大鼠SMA血管管径舒张和收缩剂NE(3 μg·kg-1)诱导的血管管径收缩没有明显的影响;而18α-GA处理可明显抑制内皮依赖的血管舒张剂ACh(2 μg·kg-1)和收缩剂杨梅黄酮(2 μg·kg-1)诱导的血管舒/缩反应,18α-GA处理组的ACh诱导的血管舒张率和杨梅黄酮诱导的管径收缩率分别降低至相应对照组的35.1%和26.8%(P<0.01)。结论 MEGJ在失血性休克大鼠内皮依赖的血管舒张/收缩功能调节中具有重要的作用。

       

      Abstract: OBJECTIVE To observe the effects of myo-endothelial gap junction(MEGJ) on the endothelium-dependent and -independent vasorelaxation/vasoconstriction of superior mesenteric artery(SMA) in hemorrhagic shock rats. METHODS With determined the changes of diameter of SMA by a intravital microscope system, the effects of 18α-glycyrrhetic acid(18α-GA), a uncoupling agent of MEGJ, on endothelium-independent vascular contractile response to norepinepherine(NE), endothelium- independent relaxation reactivity to sodium nitroprusside(SNP), and endothelium–dependent contractile response to myricetin, endothelium-dependent relaxation reactivity to acetylcholine(ACh) in hemorrhagic shock rats were observed. RESULTS After treatment with 18α-GA(2 mg·kg-1), the endothelium-independent vasorelaxation/vasoconstriction of SMA induced by SNP (10 μg·kg-1) or NE(3 μg·kg-1) in hemorrhagic shock rats had no significant changes. While 18α-GA pretreatment significantly blocked the endothelium-dependent relaxation reactivity to ACh(2 μg·kg-1) and contractile response to myricetin(2 μg·kg-1), the vascular relaxation/contractile response of SMA to ACh or myricetin in 18α-GA group were decreased to 35.1% and 26.8% of the control group, respectively(P<0.01). CONCLUSION MEGJ played important role in the regulation of endothelium-dependent vasorelaxation/vasoconstriction in hemorrhagic shock rats.

       

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