1 The mechanisms by which the bile salt, sodium taurocholate, potentiates the formation of gastric mucosal erosions induced by indomethacin has been investigated in the rat.
2 Systemic administration of indomethacin lowered resting mucosal blood flow but had no effect on the acid back‐diffusion across the mucosa.
3 Gastric perfusion of taurocholate in acid solution increased acid back‐diffusion and lowered the potential difference. This was accompanied by an increase in mucosal blood flow, which may represent a protective mechanism in the mucosa.
4 Administration of indomethacin during acid‐taurocholate perfusion reduced this elevated mucosal blood flow without any further change in acid back‐diffusion.
5 The results suggest that although a decrease in mucosal blood flow or an increase in acid back‐diffusion can lead to a low incidence of erosions, a combination of both produces extensive mucosal damage.
6 The (15S)‐methyl analogue of prostaglandin E2 reduced erosion formation induced by indomethacin and acid‐taurocholate administration.
7 It is suggested that this protective action of the prostaglandin analogue may be linked to changes in gastric mucosal permeability and in mucosal blood flow.
DOI: 10.1111/j.1476-5381.1977.tb07522.x
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