高渗盐水致大鼠萎缩性胃炎胃黏膜扫描电镜观察

Scanning electromicroscope observation of gastric mucosa with atrophic gastritis caused by salt water in rats

目的研究高渗盐水灌胃导致大鼠萎缩性胃炎(CAG)胃黏膜组织病理变化及细胞超微结构变化,探讨长期咸饮食与慢性萎缩性胃炎发生的关系。方法用盐水灌胃(25℃15%盐水灌胃,1次/d,2.5m l/次)建立大鼠萎缩性胃炎动物模型。选取大鼠腺胃胃窦组织进行病理组织学检查,以扫描电镜观察胃黏膜上皮细胞超微结构的变化。结果光镜下见高渗盐水灌胃后第24周,大鼠胃黏膜出现腺体明显缩小,黏膜肌层的平滑肌呈束状增生插入黏膜固有层中。腺体上1/3至2/3腺上皮萎缩,腺管腔增宽,胃小凹颈部黏膜宽度变窄。扫描电镜见正常组大鼠胃黏膜被纵横交错的小沟分隔成许多胃小区,呈网状,胃小凹(胃腺开口)壁衬有圆形或椭圆形上皮细胞,体积基本一致,有短而稀的微绒毛。上皮细胞排列规则,被覆一薄层连续的粘液。盐水组大鼠在24周时胃黏膜表面扁平,腺细胞表面粗糙,腺腔间黏膜变宽;并见局限性黏膜剥脱,剥脱后的黏膜腺体萎缩,腺腔增大;到32周时,见胃黏膜上皮细胞萎缩、腺腔直径增大、细胞表面破溃,出现大小不等、形状不规则的糜烂面并见纤维性渗出。结论盐水灌胃可引起胃黏膜组织细胞损害,长期过咸刺激可损伤胃黏膜诱发黏膜萎缩。

Objective To observe the tissular pathological and ultrastructural changes of gastrie mucosa with experimental atrophic gastritis caused by salt-water in rats and to explore the relationship between atrophic gastritis and high-salt diet. Methods The atrophic gastritis rat model was made by salt-water perfusion（0. 15g/ml, 2. 5mL/d ）. The tissue of sinus ventriculi was detected with histopathologic examination and the ultrastructure of gastric mucosa was observed by scanning electron microscope. Results Under light microscope, the gastric gland was shrunk obviously in high-salt water perfusion group after high-salt water was given for 24 weeks. The muscle in muscular layer was hyperplasia and cramped into the lamina propria. The glandular epithelium in the upper 1/3 -2/3 edge of the gland was atrophic. The gastric micro-depression became broaden and the width of cervical part of gastric pit became narrow. Under the scanning electroroicroscope, the gastric mucosa was comparted into many gastric areas in the control group. Round or elliptic epithelium cells lined on the wall of gastric pits were in the same size and had short and spare microvillus. The epithelium was lined regularly and covered by laminar mucus. In salt-water perfusion group after the salt-water was given for 24 weeks, the surface of the gastric mucosa became thin and flat, and the glandular cells became rough, The mucosa between lumens of gland was broadened and the limited exfoliation of mucosa also could be seen. When the salt-water was given for 32 weeks, the gastric epithelial cells were shrunk, and the diameter of lumen of gland was broadened. There was breakage in the cell surface. Erosions with various size and shape and fibrous exudation could be seen. Conclusion Salt-water perfusion may cause the damage of the epithelia of gastric mucosa in experimental rats and long- term high-salt stimulation can induee the injury and atrophy of gastric mucosa.