| 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. |
