组织胺通过H_2受体抑制前列腺素E_2刺激家兔十二指肠碳酸氢的分泌

INHIBITION OF PGE2-STIMULATED DUODENAL BICARBONATE SECRETION BY HISTAMINE THOUGH H2-RECEPTOR IN RABBITS

十二指肠粘膜分泌的碳酸氢（ＨＣＯ３）是重要的“防御因子”之一。前列腺素Ｅ２（ＰＧＥ２）强烈刺激十二指肠ＨＣＯ３的分泌。本实验示，组织胺可抑制家兔近端十二指肠由ＰＧＥ２刺激引起的ＨＣＯ３－分泌（从０．４０±０．０３至０．０８±０．０ｌμｏｌ／ｃｍ２·ｈ，Ｐ＜０．０１）。此抑制作用可被神经毒素（ＴＴＸ）及Ｈ２受体拮抗剂一西咪替丁阻断（分别为０．３７±０．０６，０．４４±０．０２μｍｏｌ／ｃｍ２·ｈ），但不能被Ｈ１及Ｈ３受体拮抗剂所阻断。提示十二指肠肥大细胞、组织胺参与其ＨＣＯ３－分泌的调节，具体环节可能通过十二指肠神经丛的Ｈ２受体。

icarbonate(HCO3) secreted by the duodenal epithelium is one of the important“defensive factors”. Patients with duodenal ulcer have impaired proximal duodenal HCO3secretion。 Prostaglandin E2(PGE2) stimulates HCO3 secretion, In rabbit,histamine essentiallyabolished PGE2-stimulated proximal duodenal mucosal HCO3 secretion in vitro (from0.40 ± 0.03 to 0.08 ± 0,0lμmol/cm2·h),an effect which could be reversed by both theneurotoxin(tetrodotoxin, TTX) and the histamine H2-receptor antagonist(cimetidine)(0.37 ± 0.06,0.44 ± 0.02μmol/cm2·h,respectively),and reproduced by the H2-receptor agonistdimaprit. The results suggested that histamine contains an anti-defensive action by inhibitionof PGE2-stimulated duodenal HCO3 secretion。