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明佳,张瑗,李涛,杨光明,徐竞,刘良明.Cx40、Cx43在失血性休克大鼠血管舒张反应调节中的作用[J].陆军军医大学学报(原第三军医大学学报),2008,30(13):1227-1230.
MING Jia,ZHANG Yuan,LI Tao,YANG Guang-ming,XU Jing,LIU Liang-ming.Regulatory role of Cx40/43 in endothelium-dependent vasorelaxation reactivity of superior mesenteric artery in hemorrhagic shock rats[J].J Amry Med Univ (J Third Mil Med Univ),2008,30(13):1227-1230.
明佳,张瑗,李涛,杨光明,徐竞,刘良明.Cx40、Cx43在失血性休克大鼠血管舒张反应调节中的作用[J].陆军军医大学学报(原第三军医大学学报),2008,30(13):1227-1230. DOI:
MING Jia,ZHANG Yuan,LI Tao,YANG Guang-ming,XU Jing,LIU Liang-ming.Regulatory role of Cx40/43 in endothelium-dependent vasorelaxation reactivity of superior mesenteric artery in hemorrhagic shock rats[J].J Amry Med Univ (J Third Mil Med Univ),2008,30(13):1227-1230. DOI:
目的 研究Cx40、Cx43在失血性大鼠肠系膜上动脉内膜依赖的血管舒张反应性调节中的作用及其可能的调节机制。 方法 以SD大鼠肠系膜上动脉(superior mesenteric artery,SMA)为研究对象,采用体外缺氧模型,以Cx40或Cx43的反义寡脱氧核苷酸(Cx40/43 antisense oligodeoxyribonucleotide
Cx40/43 AODN)阻断SMA的Cx40或Cx43表达,观察Cx40/43 AODN对缺氧处理SMA舒张反应性、MLCP和MLCK活性等的影响。 结果 Cx40 AODN可以显著增加SMA内膜依赖的舒张反应性(P0.01);Cx43 AODN可以显著降低SMA内膜依赖的舒张反应性(P0.01)。Cx40/43 AODN对SMA的MLCK、MLCP活性无明显作用。 结论 Cx40和Cx43参与了失血性休克后内膜依赖的血管舒张反应性的调节,其机制与血管的MLCK和MLCP活性无明显关系。
Objective To investigate the role and possible mechanism of Cx40/43 regulating the endothelium-dependent vasorelaxation reactivity following hemorrhagic shock in rats. Methods Superior mesenteric arteries (SMAs) was taken out from SD rats
and cut into 2-3 mm segments. Cx40/43 antisense oligodeoxyribonucleotide (Cx40/43 AODN) was transfected into the segments respectively
and then the transfected and non-transfected segments were cultured in a hypoxia culture tank. The changes of vasodilation response
the activities of myosin light chain kinase (MLCK) and myosin light chain phosphatase (MLCP) were observed. Results Cx40 AODN improved the vasorelaxation response of SMA
while Cx43 AODN attenuated it. Cx40/43 AODN had no effect on the MLCK and MLCP activities of SMA. Conclusion Both Cx40 and Cx43 have important effects on regulating the endothelium-dependent vasorelaxation reactivity in rats following hemorrhagic shock. The regulation has no relation with the activities of MLCP and MLCK of SMAs.
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