兔失血性休克再灌注小A的形态学观察及α-SMA、ICAM-1的表达
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摘要
目的观察新西兰大白兔失血性休克再灌注后小动脉的形态学改变,探索α-SMA、ICAM-1在再灌注后不同时点的表达与小动脉的形态改变的关系。方法将35只新西兰大白兔分为(1)对照组;(2)急性失血性休克25分钟组;(3)失血休克再灌注3/4小时组;(4)失血休克再灌注1小时组;(5)失血休克再灌注2小时组;(6)失血休克再灌注3小时组;(7)失血休克再灌注4小时组,依次分为A组、B组、C组、D组、E组、F组、G组,各组均为5只;失血休克再灌注各组在急性失血性休克25分钟后由静脉缓慢回输所抽动脉血及等量生理盐水,取心、脑、肾、空肠及下肢小动脉,用光镜和透射电镜观察小动脉内皮细胞和平滑肌细胞的形态,同时用免疫组织化学的方法显示α-SMA、ICAM-1在小动脉内皮细胞和平滑肌细胞中的表达。结果1.光镜下和电镜下见B组的小动脉内皮细胞个别脱落,平滑肌细胞轻微水肿。再灌注后内皮细胞坏死脱落、血管平滑肌细胞水肿明显,平滑肌细胞向内膜迁移,再灌注1小时损伤最显著。脑皮质与其他组织小动脉相比较,在缺血再灌注后不同时点的损伤较轻。再灌注3小时后逐渐恢复。2.A组α-SMA各组织均适度表达,B组α-SMA表达降低,再灌注1小时达到最低,再灌注3小时表达增加。D组、E组、F组、G组和A组比较,差异均有统计学意义(P<0.05)。3.A组ICAM-1有少量表达,B组ICAM-1表达首先增加,再灌注后4小时达到高峰。D组、E组、F组、G组和A组比较,差异均有统计学意义(P<0.05)。结论1.新西兰大白兔失血性休克再灌注小动脉内皮细胞和平滑肌细胞损伤各时间点表现不同。2.α-SMA的表达在各实验组与A组比较中有统计学差异(P<0.05),提示α-SMA与血管平滑肌细胞的舒缩状态有密切的关系,平滑肌细胞在再灌注各时点处于不同的收缩状态;ICAM-1的表达在各实验组与A组比较中有统计学差异(P<0.05),提示缺血再灌注具有炎症反应的特征是由于ICAM-1在内皮细胞表达升高造成的,再灌注炎症反应致使内皮细胞肿胀,小动脉内径缩小,导致血流灌注量减少。
Objective To objective the morphological changes of small artery after hemorrhagic shock and resuscitation in rabbits and expression ofα-SMA、ICAM-1. Methods Specimen of tissues were taken in the ischemia 25 minutes and reperfusion for 3/4、1、2、3、4 hours. By light microscope and electron microscope, observes the morphological changes of small artery. Though the immunohistochemistry technique to observe the expression ofα-SMA and ICAM-1. Results 1. Light microscope: The injury degree of reperfusion was more sever than ischemia group.2.Electron microscope: There are morphological changes of small artery in 25 min ischemia group, presenting mainly as endothelial cells swelling, abnormal nucleus, karyotin manifold and lie in side; smooth muscle cells karyotheca crimple, karyotin manifold and with bubbles inside. The injury degree of reperfusion was more severe than ischemia group. The most severe cellular damage was found in 1 hour after reperfusion.3. The normal control groupα-SMA organizations have expressed. But the expression ofα-SMA in the ischemia and reperfusion was changed successively. The expression ofα-SMA was decreased after ischemia 25 min; reperfusion one hour to meet minimum, and began to increase gradually after reperfusion for 3 hours.4.The expression of ICAM-1 was little increased in the normal group. The expression of ICAM-1 was increased after ischemia 25 min; it peaked after reperfusion for 4 hour. Conclusion 1. Hemorrhagic shock and resuscitation can induce morphological changes of small artery; it can induce hemorrhagic shock reperfusion damage of small artery. 2.α-SMA expression of the acute phase of ischemia and hypoxia and recovery vessel configuration, activity and function have a certain significance. The hemorrhagic shock reperfusion damage of small artery was possible induced by ICAM-1.
Objective To objective the morphological changes of small artery after hemorrhagic shock and resuscitation in rabbits and expression ofα-SMA、ICAM-1. Methods Specimen of tissues were taken in the ischemia 25 minutes and reperfusion for 3/4、1、2、3、4 hours. By light microscope and electron microscope, observes the morphological changes of small artery. Though the immunohistochemistry technique to observe the expression ofα-SMA and ICAM-1. Results 1. Light microscope: The injury degree of reperfusion was more sever than ischemia group.2.Electron microscope: There are morphological changes of small artery in 25 min ischemia group, presenting mainly as endothelial cells swelling, abnormal nucleus, karyotin manifold and lie in side; smooth muscle cells karyotheca crimple, karyotin manifold and with bubbles inside. The injury degree of reperfusion was more severe than ischemia group. The most severe cellular damage was found in 1 hour after reperfusion.3. The normal control groupα-SMA organizations have expressed. But the expression ofα-SMA in the ischemia and reperfusion was changed successively. The expression ofα-SMA was decreased after ischemia 25 min; reperfusion one hour to meet minimum, and began to increase gradually after reperfusion for 3 hours.4.The expression of ICAM-1 was little increased in the normal group. The expression of ICAM-1 was increased after ischemia 25 min; it peaked after reperfusion for 4 hour. Conclusion 1. Hemorrhagic shock and resuscitation can induce morphological changes of small artery; it can induce hemorrhagic shock reperfusion damage of small artery. 2.α-SMA expression of the acute phase of ischemia and hypoxia and recovery vessel configuration, activity and function have a certain significance. The hemorrhagic shock reperfusion damage of small artery was possible induced by ICAM-1.
引文
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