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目的建立冷-束缚应激(CRS)诱导肠黏膜屏障破坏大鼠模型,探讨肠黏膜屏障变化在应激发病机制中的作用。方法选取W istar大鼠40只,随机分成模型组和正常对照组。模型组采用寒冷加束缚为应激源实施干预,对照组不予任何干预。实验期间通过直结肠扩张(CRD)实验测定内脏敏感性,取大鼠远端结肠及回肠黏膜行病理组织学检查。采用气相色谱法(GC)测定两组大鼠5h尿液中乳果糖(L)与甘露醇(M)排泄率(L/M)比值,反映肠黏膜屏障的变化情况。8结果模型组初始感觉阈值、疼痛感觉阈值、最大耐受阈值分别较对照组显著降低(P<0.05);两组肠黏膜病理检查均未见明显异常;模型组大鼠5 h尿液中L/M比值较对照组显著增大(P<0.05)。结论应激损伤导致大鼠肠黏膜通透性增大,肠黏膜屏障受损可能与应激发病机制有关。
Objective To establish a rat model of intestinal mucosal barrier disruption induced by cold-restraint stress (CRS) and investigate the role of intestinal mucosal barrier changes in the pathogenesis of stress. Methods 40 Wistar rats were randomly divided into model group and normal control group. In the model group, cold and restraint were used as the stress source for intervention, and the control group received no intervention. During the experiment, the visceral sensitivity was measured by the method of direct colonic dilatation (CRD). The histopathological examination of distal colon and ileum mucosa was performed. The ratio of lactate (L) and mannitol (M) excretion (L / M) in urine of 5h group was measured by gas chromatography (GC) to reflect the change of intestinal mucosal barrier. 8 Results The initial sensory threshold, pain sensation threshold and maximum toleration threshold of the model group were significantly lower than those of the control group (P <0.05). No significant abnormalities were observed in pathological examination of intestinal mucosa between the two groups. In model group, L / M ratio was significantly higher than the control group (P <0.05). Conclusion Stress injury leads to increased intestinal mucosal permeability and impaired intestinal mucosal barrier, which may be related to the pathogenesis of stress.