DISTENTION-INDUCED GASTRIN-RELEASE - EFFECTS OF LUMINAL ACIDIFICATION AND INTRAVENOUS ATROPINE

Abstract

Whether gastric distention with saline test meals could release gastrin in healthy subjects and whether luminal acidification or atropine would modify this response were studied. Distention with 700 ml saline adjusted to pH 5.0 led to a significant gastrin response (averaging 9 .+-. 3 pg/ml above based levels during the first 14 min after distention, P < 0.02), whereas distention with 25 ml saline led to no gastrin release. Distention with 700 ml saline adjusted to pH 2.5 also led to a significant gastrin rise, which was nearly identical to that seen at pH 5.0. A small dose of atropine (2.3 .mu.g/kg i.v.) significantly enhanced the gastrin response to 700-ml distention at pH 5.0 (average gastrin rise 20 .+-. 3 pg/ml, P < 0.02 vs. 700 ml without atropine). This enhancement of gastrin release by atropine was not due to changes in intragastric pH, become pH was held constant at 5.0 by in vivo inttragastric titration. Enhancement was also not due to greater gastric distention after atropine, because gastric volume after the 700-ml test meal were similar with or without atropine. Although atropine enhanced distention-induced gastrin release, atropine reduced acid secretion by more than 50% (P < 0.05). Gastric distention releases significant amounts of gastrin in healthy subjects; this gastrin response is resistant to inhibition by luminal acidification to pH 2.5 and the gastrin response to distention is enhanced by atropine, suggesting that distention may also activate cholinergic pathways that inhibit gastrin release.