Abstract
In an attempt to elucidate which mechanisms of mucus barrier breakdown are important in the formation of gastric erosions, changes occurring in the epithelial mucin content of gastric mucosa exposed to a damaging agent were studied quantitatively. Male Wistar rats (n = 30) were starved for 24 h, then dosed orally with aspirin suspension (300 mg/kg body weight). Animals were killed after 3, 5 or 9 h. Paraffin sections of gastric mucosa were prepared from each and were stained with Alcian blue pH 2.5 (for acidic glycoproteins) or PAS (neutral glycoproteins). Control animals (n = 15) were treated identically, apart from the omission of aspirin from the suspension. The mean integrated optical density (IOD) of each slide was measured using a Vickers M85 Microdensitometer. The mean IOD for PAS-stained sections dropped to 50% of the control value in the 3-h group (P less than 0.001), returning to 84% of the control value in the 5-h group and normal in the 9-h group. In contrast, mean IOD for Alcian blue stained sections was only marginally reduced after 3 h, but showed considerable reduction in the 5-h (57% of control value) and 9-h (61% of control value) groups. It is suggested that this diminished epithelial mucin content is a consequence of cellular exfoliation. Such depletion of epithelial mucin content represents a diminished source of supply for the surface gel, the reduced thickness of which would compromise the 'mucus-bicarbonate' barrier.
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