Abstract
Although many substances break the physiological gastric mucosal barrier, little is known regarding their ultrastructural sequelae. We selected for morphological study two dissimilar barrier breakers—ethanol and urea. Fasted Swiss mice received, via esophageal intubation, ethanol, urea, or control solutions for periods up to 15 min. Both ethanol and urea produced morphological changes in some animals as early as after 2-min exposure. The first observable effects of ethanol involved nuclear and cytoplasmic changes within the surface mucous cell without apparent disruption of the apical cell membrane or tight junction. We infer from these findings that the lipid solubility of ethanol may allow it to diffuse rapidly through the apical membrane or tight junction without causing appreciable damage until it is within the cell. In contrast, urea solutions initially caused distortion of the tight junctions and formation of vacuoles within the surface mucous cell, while the remainder of the cell appeared normal. These observations suggest that urea, being relatively impermeant across gastric epithelium, may cause injury via osmotic forces. These studies indicate that, although different gastric mucosal irritants produce similar physiological effects, they are not uniform in their morphological sequence of injury.
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