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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(10μg.kg-1)诱导的失血性休克大鼠SMA血管管径舒张和收缩剂NE(3μg.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(2μg.kg-1)和收缩剂杨梅黄酮(2μg.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。
Objective To investigate the role of the myo-endothelial gap junction (MEGJ) channel in the regulation of endothelium-dependent and endothelium-dependent vasoconstriction / diastolic function of the superior mesenteric artery (SMA) in hemorrhagic shock rats. METHODS: The effects of 18α-glycyrrhetinic acid (18α-GA), a blocker of MEGJ, on the expression of norepinephrine (NE) and diastolic sodium nitroprusside (SNP), a non-endothelium dependent vasoconstrictor, , As well as its effects on vasorelaxation and / or vasorelaxation in shock-induced shock rats induced by myricetin, an endothelium-dependent vasoconstrictor, and diastolic acetylcholine (ACh). RESULTS: 18α-GA (2 mg · kg-1) attenuated SMA vascular diameter relaxation and neutrophil NE (3 μg · kg-1) induced by non-endothelium dependent vasodilator SNP ) Induced vasoconstriction did not have a significant effect; while 18α-GA treatment could significantly inhibit the vasoconstriction induced by endothelium-dependent vasodilator ACh (2μg.kg-1) and contractile myricetin (2μg.kg-1) ACh-induced vasodilatation and myricetin-induced diameter-shrinkage in 18α-GA treatment group decreased to 35.1% and 26.8% (P <0.01) of the corresponding control group, respectively. Conclusion MEGJ plays an important role in the regulation of endothelium-dependent vasodilation / contraction in hemorrhagic shock rats.