The potentiation of taurocholate‐induced rat gastric erosions following parenteral administration of cyclo‐oxygenase inhibitors

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Abstract
Subcutaneous administration of anti‐inflammatory doses of aspirin, indomethacin, naproxen and flurbiprofen inhibited prostacyclin formation ex vivo in the luminally‐perfused gastric mucosa of anaesthetized rats. These doses of anti‐inflammatory compounds potentiated the formation of gastric mucosal erosions following 3 h luminal perfusion of the topical irritant, acidified sodium taurocholate (2 mm in 100 mm HCl). The increase in luminal acid‐loss during gastric perfusion of acidified taurocholate was not significantly enhanced by these anti‐inflammatory agents. A correlation was found between the increase in gastric erosion formation and the inhibition of mucosal prostacyclin formation ex vivo by intravenous injection of aspirin or ketoprofen during acid‐taurocholate perfusion. BW755C, which failed to inhibit mucosal prostacyclin formation ex vivo, did not significantly augment acid‐taurocholate induced gastric damage. The present findings support the potentiating interactions between topical irritation and inhibition of gastric cyclo‐oxygenase in the genesis of the gastric lesions.