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RELATIONSHIP BETWEEN LESION FORMATION AND PERMEABILITY OF RAT GASTRIC MUCOSA TO H + AND OTHER CATIONS
Author(s) -
BUNCE K.T.,
McCARTHY J.J.,
SPRAGGS C.F.,
STABLES R.
Publication year - 1982
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.1476-5381.1982.tb08790.x
Subject(s) - aspirin , gastric mucosa , chemistry , lesion , medicine , prostaglandin e2 , prostaglandin , in vivo , permeability (electromagnetism) , endocrinology , pharmacology , pathology , stomach , biochemistry , biology , microbiology and biotechnology , membrane
1 The relationship between lesion formation and ionic permeability has been investigated in rat gastric mucosa in vivo . Changes in these parameters were measured in the mucosa treated topically with prostaglandins E 2 and A 2 and/or aspirin. Particular attention was paid to the net flux of H + ions across the gastric mucosa. 2 The effect of aspirin concentrations of 5 m m , 20 m m and ‘40 m m ’ (the latter, a suspension in a saturated solution) was investigated. Aspirin concentrations of 20 m m and ‘40 m m ’ produced a marked increase in lesion formation and increased the net mucosal to serosal flux of H + ions. Aspirin 5 m m produced a significant increase in lesion formation but did not cause a significant change in net H + ion flux. This result suggests that aspirin can have a direct irritant effect on the gastric mucosa and that the back diffusion of H + ions is not a pre‐requisite for the development of overt mucosal ulceration. 3 The effect of topically applied prostaglandin E 2 (PGE 2 ) on aspirin‐induced gastric mucosal damage was investigated. Concentrations of PGE 2 of 10 −5 m and 10 −4 m ameliorated aspirin‐induced damage, but these changes were not necessarily accompanied by a significant reduction in net H + ion flux. Again, this result is not consistent with a direct relationship between lesion formation and mucosal permeability to H + ions. 4 Since PGA 2 did not ameliorate aspirin‐induced mucosal damage, the protective effect of PGE 2 could not be attributed to its conversion to PGA 2 in the acidic environment of the gastric lumen. 5 Changes in gastric mucosal potential difference (p.d.) and net fluxes of Na + and K + ions may occur without a concomitant change in the permeability of the gastric mucosa to acid back‐diffusion. Thus, the assumption cannot be made that a change in the permeability of the gastric mucosa to one particular ion reflects a general increase in ionic permeability.