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目的 :探讨应激条件下大鼠胃壁细胞泌酸功能和超微结构的动态变化及与急性胃粘膜损伤之间的关系。方法 :将 32只雄性SD大鼠随机分成 4组 ,即对照组、水浸束缚应激 1,2、4h组。检测各组胃液pH值、胃粘膜溃疡指数 (UI) ,并取腺胃区粘膜制作透射电镜标本 ,观察壁细胞超微结构变化。结果 :应激条件下大鼠胃泌酸多于对照组 ,随应激时间延长胃液pH值明显低于对照组 (P <0 0 1) ;UI随应激时间延长明显增加 (P <0 0 1) ,与pH值之间呈明显负相关 (r=- 0 9987,P <0 0 1) ;电镜下见对照组壁细胞呈静息状态 ,而应激 1、2、4h组壁细胞呈现不同的激活状态 ,且以 4h为明显 ,壁细胞内线粒体丰富 ,分泌小管密集 ,囊管泡减少或消失 ,呈明显泌酸活跃状态。结论 :水浸束缚应激可引起大鼠胃酸分泌增加 ,这与壁细胞超微结构改变相一致 ,并与胃粘膜损伤程度有明显相关性。提示胃酸在应激性溃疡的发生发展过程中具有重要意义。
Objective: To investigate the dynamic changes of acid secretion and ultrastructure in rat gastric parietal cells under stress and its relationship with acute gastric mucosal injury. Methods: Thirty-two male Sprague-Dawley rats were randomly divided into 4 groups: control group, water immersion restraint stress for 1, 2 and 4 hours. Gastric juice pH value and gastric mucosal ulcer index (UI) of each group were measured. Transmission electron microscopy was performed on the gastric mucosa to observe the ultrastructure of parietal cells. Results: Compared with the control group, the gastric acid secretion in rats under stress was significantly higher than that in the control group (P <0 0) 1), and negatively correlated with the pH (r = - 0 9987, P <0.01). In the control group, the parietal cells were in resting state, Different activation state, and to 4h obvious, parietal cells rich in mitochondria, secretory tubules dense, vesicular vacuoles reduce or disappear, was significantly acid-activated state. Conclusion: Immersion restraint stress can cause gastric acid secretion increase, which is consistent with the changes of parietal cells ultrastructure, and gastric mucosal injury has a significant correlation. It suggests that gastric acid is of great significance in the development of stress ulcer.