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前列腺素、一氧化氮和血管活性肠肽在调节十二指肠碱性分泌和运动中的相互作用。

Interaction between prostanoids, NO, and VIP in modulation of duodenal alkaline secretion and motility.

作者信息

Sababi M, Hällgren A, Nylander O

机构信息

Department of Physiology and Medical Biophysics, Uppsala University, Sweden.

出版信息

Am J Physiol. 1996 Oct;271(4 Pt 1):G582-90. doi: 10.1152/ajpgi.1996.271.4.G582.

DOI:10.1152/ajpgi.1996.271.4.G582
PMID:8897876
Abstract

The relation between duodenal motility and duodenal mucosal alkaline secretion (DMAS) was examined in anesthetized rats. The duodenum was perfused with saline, and DMAS was determined by titration. Duodenal motility, assessed by intraluminal pressure measurements, was induced by indomethacin and/or N omega-nitro-L-arginine methyl ester (L-NAME) and inhibited by iloprost or vasoactive intestinal peptide (VIP). Six of 66 rats showed spontaneous duodenal contractions. Basal DMAS was higher in these rats than in those without contractions. Rats treated with indomethacin and L-NAME before abdominal operation exhibited duodenal motility postoperatively and had higher DMAS than in controls. Iloprost abolished both the duodenal motility increase and increase in DMAS induced by indomethacin. L-NAME-induced motility and increase in DMAS were antagonized by L-arginine. VIP increased DMAS without affecting motility. VIP abolished indomethacin-induced motility and augmented indomethacin-stimulated DMAS. VIP reduced L-NAME-induced motility and slightly increased L-NAME-stimulated DMAS. It is concluded that DMAS varies with duodenal motility. Prostaglandins and NO inhibit duodenal motility, thereby indirectly reducing DMAS. VIP may have dual effects on DMAS, an inhibitory action mediated via smooth muscle relaxation and a stimulatory action independent of motility.

摘要

在麻醉大鼠中研究了十二指肠运动与十二指肠黏膜碱性分泌(DMAS)之间的关系。用生理盐水灌注十二指肠,并通过滴定法测定DMAS。通过腔内压力测量评估的十二指肠运动由吲哚美辛和/或Nω-硝基-L-精氨酸甲酯(L-NAME)诱导,并被伊洛前列素或血管活性肠肽(VIP)抑制。66只大鼠中有6只出现自发性十二指肠收缩。这些大鼠的基础DMAS高于无收缩的大鼠。腹部手术前用吲哚美辛和L-NAME治疗的大鼠术后表现出十二指肠运动,且DMAS高于对照组。伊洛前列素消除了由吲哚美辛诱导的十二指肠运动增加和DMAS增加。L-NAME诱导的运动和DMAS增加被L-精氨酸拮抗。VIP增加DMAS而不影响运动。VIP消除了吲哚美辛诱导的运动并增强了吲哚美辛刺激的DMAS。VIP降低了L-NAME诱导的运动并略微增加了L-NAME刺激的DMAS。结论是DMAS随十二指肠运动而变化。前列腺素和NO抑制十二指肠运动,从而间接降低DMAS。VIP可能对DMAS有双重作用,一种通过平滑肌松弛介导的抑制作用和一种独立于运动的刺激作用。

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