Role of taurocholic acid in production of gastric mucosal damage after ingestion of aspirin.
The possibility that aspirin-induced gastric mucosal damage may occur more readily in the presence of bile has been studied in man using measurement of transmucosal electrical potential difference as a marker of disruption of the gastric mucosal barrier. After the introduction of acetylsalicylic acid (600 mg) in suspension to seven subjects the mean electrical potential difference (plus or minus S.E. of mean) fell significantly from -33-3 plus or minus 2-0 mV to - 17-1 plus or minus 2-1 mV, and after the introduction of taurocholic acid (5 mmol/1) to seven other subjects the electrical potential difference fell significantly from -38-1 plus or minus 3-0 mV to-19-1 plus or minus 3-4 mV, the mean duration of these changes being 14-4 and 17-5 minutes respectively. When a combination of acetylsalicylic acid and taurocholic acid was introduced to eight subjects the mean electrical potential difference also fell significantly from -38-6 plus or minus 1-8 mV to -17-9 plus or minus 1-8 mV, but mean duration of this change (27 minutes) was significantly longer than that found after acetylsalicylic acid or taurocholic acid alone. These results indicate that the ingestion of aspirin, together with coincidental reflux of bile from duodenum, may be a factor in the pathogenesis of aspirin-induced gastric mucosal damage.
D001241:Aspirin / Q000009:adverse effects / Q000494:pharmacology; D001646:Bile / Q000378:metabolism; D004357:Drug Synergism; D005753:Gastric Mucosa / Q000187:drug effects*; D006801:Humans; D008564:Membrane Potentials / Q000187:drug effects; D013272:Stomach Diseases / Q000139:chemically induced; D013656:Taurocholic Acid / Q000494:pharmacology* / Q000502:physiology
D013656:Taurocholic Acid; D001241:Aspirin