Morphologic basis of the functional gastric acid barrier.
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.
Pabst
M A
MA
Department of Histology and Embryology, University of Graz, Austria.
Wachter
C
C
Holzer
P
P
D000818:Animals; D001485:Basement Membrane / Q000187:drug effects / Q000648:ultrastructure; D004305:Dose-Response Relationship, Drug; D004848:Epithelium / Q000187:drug effects / Q000648:ultrastructure; D000431:Ethanol / Q000494:pharmacology; D005260:Female; D005753:Gastric Mucosa / Q000187:drug effects / Q000502:physiology* / Q000648:ultrastructure*; D006851:Hydrochloric Acid / Q000494:pharmacology*; D008833:Microcirculation; D008854:Microscopy, Electron; D008855:Microscopy, Electron, Scanning; D051381:Rats; D017207:Rats, Sprague-Dawley
D000431:Ethanol; D006851:Hydrochloric Acid