重复正加速度暴露对大鼠心肌血管内皮超微结构和ICAM-1表达的影响

CHANGES OF ULTRASTRUCTURE IN CARDIOVASCULAR ENDOTHELIUM AND ITS ICAM-1 EXPRESSION IN RAT AFTER REPETITIVE POSITIVE ACCELERATION EXPOSURES

目的 :观察重复正加速度 (+Gz)暴露对大鼠心肌血管内皮细胞超微结构的影响及其暴露后细胞间粘附分子 1(ICAM 1)表达的变化情况 ,进一步探讨高 +Gz暴露致心肌损伤的机理。方法 :30只雄性Wistar大鼠随机分成 3组 (n =10 ) ,其中对照组不受 +Gz作用 ;正加速度组分为 +1Gz组 :受 +1Gz作用 ,+10Gz组 :重复 +10Gz暴露 (+10Gz 30s,5counts/d ,3d/w ,3w)。于末次 +Gz作用后次日同时处死大鼠 ,速取左室心肌 ,常规透射电镜制样、观察。另取左室心肌制成石蜡切片 ,行免疫组化检测。结果 :重复 +10Gz作用后 ,心肌间质弥漫水肿 ,小血管内皮细胞肿胀 ,吞饮泡增多 ,血管内皮细胞ICAM 1含量也明显增加 (P <0 .0 5 ) ,而 +1Gz组心肌血管内皮结构及其I CAM 1含量与对照组之间无明显差别。结论 :重复 +Gz暴露后 ,大鼠心肌血管内皮细胞可出现明显损伤 ,其I CAM 1表达增多 ,提示粘附分子诱导的炎症反应参与了高

Aim: To observe the change of cardiovascular endothelium's ultrastructure and its intercelluar adhesion molecules 1(ICAM 1) expression in rat after repetitive high positive acceleration(+Gz) exposures and further to explore the mechanisms of myocardial injuries induced by high +Gz stress. Methods: Thirty male Wistar rats were randomly divided into three groups: control group, +1Gz group and +10Gz group ( n =10 for each). The rats of +10Gz group were exposed to five plateaus at +10Gz for 30s with +1Gz 1min intervals, 3 times a week, for 3 weeks, while rats of +1Gz group subjected to +1Gz for 5mim daily. The control group didn't undergo acceleration stress. The rats were decapitated in the next day after the last centrifuge run and myocardium were immediately dissected from left ventricles for ultrastructural examination using transmission electron microscope and immunohistochemical staining of ICAM 1. Results: The ultrastructural changes of the cardiovascular endothelium were observed in rats of 10Gz group, including endothelium edema and platelet aggregating in lumen of blood vessel.Also,the expression of ICAM 1 in +10Gz stressed rats increased significantly ( P <0.05).While there was no difference between control group and +1Gz group in ultrastructure of cardiovascular endothelium and its ICAM 1 expression. Conclusion: The results suggested that repeated high +Gz exposures could injury cardiovascular endothelium of rat and increase ICAM 1 expression, which indicated cell adhesion molecules(CAMs) inducing inflammation took part in myocardial injuries induced by high +Gz stress.