急性缺血性脑卒中时胃黏膜细胞凋亡和胃屏障损伤的关系

目的评估缺血性脑卒中应激时胃黏膜细胞凋亡的状况,探讨胃黏膜细胞凋亡和胃屏障形态学和功能的关系。方法10只犬制作缺血性脑卒中模型,另10只伪手术对照。制模后检测胃蔗糖通透性,24h后取全胃行大体病理分级和组织学积分,同时测定胃黏膜上皮细胞凋亡指数。结果实验组和伪手术组相比,胃黏膜细胞凋亡显著增加(14·83±4·41vs·5·60±2·61,P<0·05);胃黏膜细胞凋亡和蔗糖通透性(r=0·89,P<0·05)、胃大体病理(r=0·87,P<0·05)、胃组织学积分(r=0·92,P<0·05)均呈正相关。结论缺血性脑卒中虽未造成全身循环呼吸等明显改变,但已引起细胞凋亡增加、胃黏膜屏障损伤,且细胞凋亡增加与屏障功能损伤、大体病理改变同步发生,提示屏障损伤的细胞基础可能与胃黏膜上皮细胞的加速凋亡相关。

Apoptosis of gastric mucosa and gastric barrier dysfunction in acute ischemic stroke

OBJECTIVE: To evaluate the role of gastric mucosa apoptosis in the stress of ischemic stroke, and to discuss the relationship between gastric mucosa apoptosis and gastric barrier. METHODS: Ten dogs were artificially made ischemic stroke by operation (IS group), and another 10 shamly-operated dogs were served as control group. Sucrose permeability were measured after the operation. All dogs were sacrificed 24 hours after operation to measure the gastric mucosal apoptosis index, gastric gross classification, and histological score. RESULTS: The gastric mucosal apoptosis index in the IS group were significantly higher than in the control group (14.83 +/- 4.41 vs. 5.60 +/- 2.61, P < 0.05). The gastric mucosal apoptosis index were correlated with the sucrose permeability (r = 0. 89, P < 0.05) , gastric gross classification (r = 0. 87, P < 0.05), and histological score (r = 0.92, P < 0.05). CONCLUSIONS: Although ischemic stroke will not cause the obvious damage in the respiratory and circulatory system, it is responsible for the apoptosis of epithelial cell in the gastric mucosa and gastric barrier dysfunction. The apoptosis index is closely correlated with the damage of the function and morphology of the gastric barrier, indicating that the epithelial cell apoptosis acceleration in the gastric mucosa may result in the damage of gastric barrier function.