Pabst M A, Wachter C, Holzer P
Department of Histology and Embryology, University of Graz, Austria.
Lab Invest. 1996 Jan;74(1):78-85.
The gastric mucosa possesses a functional barrier that prevents intrusion of luminal acid. The aim of the present study was to elucidate the morphologic basis of this barrier by exploring the effect of acid challenge on the gastric mucosal epithelium, basal lamina, and microvasculature. The stomachs of urethane-anesthetized rats were perfused, for at least 45 minutes, with 0.05 M HCl or 0.15 M HCl in the absence or presence of the mucosal barrier breaker ethanol (15%) and examined by light, scanning, and transmission electron microscopy. Gastric perfusion with 0.05 M HCl alone caused superficial cell injury, the damaged surface cells loosing the surface membrane, whereas the junctional complex and basolateral membrane were preserved. Perfusion of 0.15 M HCl alone led to focal ablation of surface epithelial cells in the interfoveolar regions, and cells in the gastric pits remained grossly normal. Exposure to the barrier breaker ethanol (15%) in the presence of 0.05 M HCl caused extensive ablation of the surface epithelium. There were many focal areas in which the honeycomb structure of the lamina propria was exposed and the basal lamina was removed. Gastric mucosal damage progressed further when the luminal HCl concentration was raised to 0.15 M in the presence of ethanol (15%). In this instance, extensive areas with deep erosions and vast areas of deep-reaching ablation of the epithelium and basal lamina were observed. Ultrastructurally, there was extensive damage to the endothelium of capillaries lying underneath denuded areas of the gastric mucosa, the injured capillaries containing erythrocyte ghosts and thrombocyte aggregates. The data suggest that the integrity of the junctional complex, basolateral membrane, and basal lamina forms the morphologic basis of the functional gastric acid barrier. Once these structures are disrupted or ablated to an appreciable extent, damage forms in the mucosal microvasculature, and injury progresses to deeper layers of the mucosa.
胃黏膜具有防止管腔内酸侵入的功能屏障。本研究的目的是通过探讨酸攻击对胃黏膜上皮、基膜和微血管系统的影响,阐明该屏障的形态学基础。用氨基甲酸乙酯麻醉大鼠,在有或无黏膜屏障破坏剂乙醇(15%)的情况下,用0.05M HCl或0.15M HCl灌注胃至少45分钟,然后通过光镜、扫描电镜和透射电镜进行检查。单独用0.05M HCl灌注胃会导致表面细胞损伤,受损的表面细胞失去表面膜,而连接复合体和基底外侧膜则得以保留。单独灌注0.15M HCl会导致胃小区间区域的表面上皮细胞局灶性剥脱,胃小凹内的细胞大体仍正常。在0.05M HCl存在的情况下暴露于屏障破坏剂乙醇(15%)会导致表面上皮广泛剥脱。有许多局灶区域,固有层的蜂窝状结构暴露,基膜被去除。当在乙醇(15%)存在的情况下将管腔内HCl浓度提高到0.15M时,胃黏膜损伤进一步进展。在这种情况下,观察到广泛的深度糜烂区域以及上皮和基膜的大面积深度剥脱区域。超微结构上,胃黏膜剥脱区域下方的毛细血管内皮有广泛损伤,受损的毛细血管含有红细胞残影和血小板聚集体。数据表明,连接复合体、基底外侧膜和基膜的完整性构成了功能性胃酸屏障的形态学基础。一旦这些结构被破坏或剥脱到相当程度,黏膜微血管系统就会形成损伤,并且损伤会进展到黏膜的更深层。