Rapid induction of gastric ulceration in guinea pigs by sequential exposure to a barrier breaker and indomethacin.
In short term experiments under halothane anesthesia, guinea pig total gastric pouches were initially and terminally exposed to 0.1 M HCl for 30 min. During an intervening 50-min test period, the gastric mucosa was exposed at pH 7.3, either to a barrier breaker (lysolecithin or diluted bile or sodium taurocholate) or to phosphate buffered saline (PBS) for half of the period, followed by exposure to indomethacin or further PBS for the second half of the test period. Scoring of mucosal damage was assessed from coded photographs and histological slides and by measurement of the transmucosal potential difference. In comparison with controls exposed only to PBS in the test period, indomethacin did produce minor but significant mucosal damage, whereas over this short time interval, the barrier breaking agents did not. Sequential exposure of pouches to lysolecithin and indomethacin caused a highly significant increase in ulceration, compared to controls or to indomethacin or lysolecithin exposure separately.
D000818:Animals; D001646:Bile / Q000502:physiology; D005753:Gastric Mucosa / Q000098:blood supply / Q000187:drug effects* / Q000503:physiopathology; D006168:Guinea Pigs; D007213:Indomethacin / Q000633:toxicity*; D008244:Lysophosphatidylcholines / Q000633:toxicity*; D013276:Stomach Ulcer / Q000139:chemically induced* / Q000473:pathology; D013656:Taurocholic Acid / Q000633:toxicity
D008244:Lysophosphatidylcholines; D013656:Taurocholic Acid; D007213:Indomethacin