肌内皮缝隙连接对失血性休克大鼠血管舒张反应的影响

Effect of myo-endothelial gap junction on vascular relaxation reactivity following hemorrhagic shock in rats

目的研究肌内皮缝隙连接对失血性休克大鼠内皮依赖和非依赖血管舒张反应的影响。方法56只SD大鼠随机分为硝普钠(SNP)组和乙酰胆碱(Ach)组,每组又分别分为正常对照组、休克0、0.5、1、2、3、4小时7个亚组;各组取其肠系膜上动脉(SMA)制成血管环,分别测量血管环在加18α-甘草次酸(18α-GA,肌内皮缝隙连接的特异性阻断剂)前、后对SNP和Ach反应性的变化。结果与正常对照组比较,各休克组SMA血管环对低浓度(10-9、10-8、10-7mol/L)SNP诱导的舒张反应明显降低;对高浓度(10-6mol/L)SNP诱导的舒张反应无明显变化;18α-GA对SNP诱导的SMA血管环的舒张反应无明显影响。休克后SMA血管环对Ach的反应呈现先下降———后增加———再下降的趋势,即休克前30分钟,SMA血管环对Ach的反应性下降,30分钟后呈上升趋势,至2小时达高峰,随后又再次下降。18α-GA可以拮抗Ach诱导的舒张反应,改变SMA血管环对Ach反应性先下降———后增加———再下降的趋势,使各休克组对Ach的反应性趋于一致。结论失血性休克后,除内皮依赖性血管舒张反应有短时间的代偿性回升外,其余的内皮依赖性和内皮非依赖性血管舒张反应在休克后均明显降低。肌内皮缝隙连接在休克后内皮依赖性血管舒张反应的变化中起重要调节作用。

Objective To observe the effect of myo - endothelial gap junction on the endothelium - dependent and -independent vascular relaxation reactivity following hemorrhagic shock in rats. Methods Fifty-six SD rats were randomly divided into sodium nitroprusside. （ SNP） and acetylcholine （ Ach） groups. Each group was respectively divided into 7 sub-groups ： normal control ,0,0.5,1,2,3 and 4h after hemorrhagic shock. Superior messenteric artery （ SMA ） was used to compare the changes of vascular response to SNP or Ach with or without 18α-glycyr rhetinic acid （18α-GA,one kind of specific myo-endothelial gap junction blocking agent）. Results Comparing with the normal control group,the vascular reactivity of SMA to SNP in each shock group was significantly decreased at lower concentration（10^-9 ,10^-8, 10^- 7mol/L ） of SNP, and had no obvious change at higher concentration（10^-6 mol/L） of SNP. 18α-GA had no effect on SNP induced SMA ringsrelaxation. The response of SMA to Ach in shock groups had a trendency of decrease - increase-decrease,which decreased in the first 30min after shock,began to in crease I h after shock,reached its peak 2h after shock,and then decreased again. 18α-GA can abolish Ach induced vascular relaxation of SMA. Conclusion The endothelium - dependent and endothelium - independent vascular relaxation response had a significant decrease following hemorrhagic shock,except a compensatory and short time in crease in endothelium - dependent vascular relaxation. Myo-endothelial gap junction plays an important role in endothelium-deoendent vascular relaxation reactivitv following hemorrhagic shock.