慢性乙醇摄取对胃粘膜损害的实验研究

Experimental Study of Chronic Gastric Mucosal Injury Induced by Ethanol Administration

目的:探索慢性乙醇摄取对胃粘膜损害的病理特点和机制。方法:按本室创建的方法用乙醇直接灌胃,于4周末、8周末和12周末分别断头处死大鼠,肉眼及镜下观察胃粘膜损伤情况、损伤指数积分及损伤程度积分。结果:模型组胃粘膜肉眼可见自糜烂到小溃疡形成,镜下由充血水肿到腺体萎缩。炎性细胞浸润的种类随时间的推移有明显不同,至4周末主要是中性粒细胞,8周末同时伴有淋巴细胞和浆细胞,而12周末在腺体萎缩的基础上主要是淋巴细胞和浆细胞。结论:长期持续乙醇刺激胃粘膜可发生腺体萎缩,同时炎性细胞浸润的种类随时间的推移有明显不同,其机制可能是胃粘膜对慢性乙醇刺激的适应性反应,主要是免疫反应。

Objective; Our aim was to determine the pathologic change and mechanism of gastric mucosal injury induced by chronic ethanol administration. Methods: Gastric mucosal injury were induced by successive intragastric etha-nol administration. The animals were killed at the end of 4, 8, 12 weeks. We observed the changes of gastric mucosa with eyes and microscope and calculated the lesion index and histologic index. Results: With the successive ethanol stimulation, body weights of models decreased significantly. Gastric mucosal was damaged in different degree, from erosion to small ulcer, from hyperemia and edema to granular atrophy. The characteristic change was that different kinds of inflammatory cells infiltrated at different stages. Neutrophil was dominant at the end of 4 weeks. Lymphocyte and plasma cell as well as neutrophil infiltrated at the end of 8 weeks. At the end of 12 weeks, granular atrophy appeared and lymphocyte and plasma cell became predominant, on the contrary, neutrophil was hardly seen. Conclusion: Long term chronic ethanol stimulation can cause granular atrophy of gastric mucosa. Different kinds of inflammatory cells infiltrate at different stages. The mechanism may be the adaption of gastric mucosa to chronic ethanol stimulation. Immunoreaction is predominant.