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幼年大鼠应激性溃疡形成机制的实验研究 被引量:1

Experimental study on mechanism of stress ulcer induced by water immersion in young rats
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摘要 目的探讨应激条件下幼鼠胃黏膜血流、自由基及肿瘤坏死因子(TNF)-α的动态变化与胃黏膜损伤之间的关系。方法采用束缚-水浸法制作应激性溃疡动物模型,将24只SD幼年大鼠随机分成4组,即对照组、水浸束缚应激45min(Ⅰ组)、90min(Ⅱ组)、3h(Ⅲ组)。检测各组胃黏膜损伤指数(UI)、胃黏膜血流量(GMBF)、血及胃组织超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量、胃组织TNF-α含量变化。结果水浸-束缚应激可导致严重胃黏膜损伤,随应激时间延长,胃黏膜UI逐渐增加,GMBF依次减低,应激幼鼠胃组织与血清中SOD活性较对照组明显降低(P〈0.01),MDA含量则明显升高(P〈0.01),应激组胃组织与血清SOD/MDA比值有降低趋势,TNF-α水平均高于对照组(P〈0.05或P〈0.01)。结论束缚-水浸应激导致幼鼠GMBF降低和微循环障碍,引起胃黏膜损伤,且应激时间越长,损伤越重,其中脂质过氧化损伤和细胞因子介导的炎症反应参与了胃黏膜损伤。 Objective To investigate the relation between the gastric mucosal injury and the dynamic structural changes of gastric mucosal blood flow (GMBF) ; free radicals and tumor necrosis factor. Methods Twenty-four SD young rats were randomly divided into four groups: control group and 45 min (Ⅰ group), 90 min (Ⅱ group), 3 h (Ⅲ group) groups under water immersion restraint stress (WRS). The change of gastric mucosal ulcer index (UI), gastric mucosal blood flow (GMBF) were observed, and the activity of SOD, the concentration of MDA and TNF-α in gastric mucosa were also detected. Results Acute gastric mucosal damage was induced by WRS, with the WRS time prolonged, UI increased gradually, GMBF and the activity of SOD in gastric mucosal and plasma remarkably decreased, and the concentration of MDA and TNF-α in gastric mucosa increased gradually in stress rats. There was significant difference in the activity of SOD, the levels of MDA and TNF-α between the stress groups and control group ( P 〈 0.05 ). Conclusion GMBF decrease and microcirculation disfunction can be induced by WRS in rat, which results in gastric mucosal ingury, and the stress time is loger, the gastric mucosal injury is worse. Lipid peroxidation injury and inflammatory mediated by cytokines in volve in the mechanism of gastric mucosal injury.
出处 《中国小儿急救医学》 CAS 2008年第1期54-57,共4页 Chinese Pediatric Emergency Medicine
关键词 应激 胃溃疡 自由基 TNF-Α Stress Gastric ulcer Free radicals TNF-α
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