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The potentiation of taurocholate‐induced rat gastric erosions following parenteral administration of cyclo‐oxygenase inhibitors
Author(s) -
Whittle B.J.R.
Publication year - 1983
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1983.tb10727.x
Subject(s) - pharmacology , prostacyclin , ex vivo , gastric mucosa , aspirin , in vivo , perfusion , flurbiprofen , medicine , chemistry , naproxen , stomach , biochemistry , in vitro , pathology , biology , alternative medicine , microbiology and biotechnology
1 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. 2 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 m m in 100 m m HCl). 3 The increase in luminal acid‐loss during gastric perfusion of acidified taurocholate was not significantly enhanced by these anti‐inflammatory agents. 4 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. 5 BW755C, which failed to inhibit mucosal prostacyclin formation ex vivo , did not significantly augment acid‐taurocholate induced gastric damage. 6 The present findings support the potentiating interactions between topical irritation and inhibition of gastric cyclo‐oxygenase in the genesis of the gastric lesions.