Hollander D, Tarnawski A, Krause W J, Gergely H
Gastroenterology. 1985 Jan;88(1 Pt 2):366-74. doi: 10.1016/s0016-5085(85)80191-8.
Histologic or ultrastructural evidence of the ability of sucralfate to protect the gastric mucosa against ethanol injury is lacking. Therefore we analyzed morphologic and functional changes in the mucosa of 120 rats receiving, intragastrically, 2 ml of either sucralfate 500 mg/kg body wt or a control solution and 1 h later 2 ml of 100% ethanol. At 15 min, 1, 4, 6, and 24 h after ethanol instillation, mucosal changes were assessed by macroscopic examination, quantitative histology, scanning electron microscopy, recordings of gastric potential difference, and measurements of volume, pH, and electrolytes in the gastric contents. Between 15 min and 24 h after ethanol instillation, macroscopic necrotic lesions in controls involved greater than 33% of mucosal area and in the sucralfate-treated group less than 4% (p less than 0.001 for each period). In controls, ethanol instillation produced surface epithelial cell disruption and deep (greater than 0.2 mm) mucosal necrosis involving greater than 55% +/- 3% of the mucosal length. In sucralfate-pretreated animals, disruption of the surface epithelium was present at 15 min, 1 h, and 4 h after ethanol instillation, but deep necrotic lesions were virtually absent (0%-2%; p less than 0.001 vs. controls) during the entire study period. The surface epithelium was mostly reestablished by 6 h after ethanol instillation in the sucralfate group but not in the controls. We concluded that sucralfate protects the gastric mucosa against ethanol-induced injury by preventing deep mucosal necrosis and as a consequence the mucosal proliferative zone cells rapidly restitute mucosal integrity.
目前缺乏硫糖铝保护胃黏膜免受乙醇损伤能力的组织学或超微结构证据。因此,我们分析了120只大鼠胃黏膜的形态学和功能变化,这些大鼠经胃内给予2ml 500mg/kg体重的硫糖铝或对照溶液,1小时后再给予2ml 100%乙醇。在乙醇灌胃后15分钟、1小时、4小时、6小时和24小时,通过宏观检查、定量组织学、扫描电子显微镜、胃电位差记录以及胃内容物的体积、pH值和电解质测量来评估黏膜变化。乙醇灌胃后15分钟至24小时,对照组的宏观坏死病变累及超过33%的黏膜面积,而硫糖铝治疗组则小于4%(每个时间段p均小于0.001)。在对照组中,乙醇灌胃导致表面上皮细胞破坏和深度(大于0.2mm)黏膜坏死,累及超过55%±3%的黏膜长度。在硫糖铝预处理的动物中,乙醇灌胃后15分钟、1小时和4小时出现表面上皮破坏,但在整个研究期间几乎没有深度坏死病变(0%-2%;与对照组相比p小于0.001)。在硫糖铝组中,乙醇灌胃后6小时表面上皮大多得以重建,而对照组则未重建。我们得出结论,硫糖铝通过防止深度黏膜坏死来保护胃黏膜免受乙醇诱导的损伤,因此黏膜增殖区细胞能迅速恢复黏膜完整性。