ROLE OF PROSTAGLANDINS AND HISTAMINE IN HYPEREMIC RESPONSE TO SUPERFICIAL AND DEEP GASTRIC-MUCOSAL INJURY AND H+ BACK-DIFFUSION IN CATS

被引：14

作者：

GISLASON, H

SORBYE, H

ABDIDEZFULI, F

WALDUM, HL

SVANES, K

机构：

[1] UNIV BERGEN,SURG RES LAB,N-5021 BERGEN,NORWAY

[2] UNIV BERGEN,DEPT BIOL CLIN,DIV ENDOCRINOL,N-5021 BERGEN,NORWAY

[3] UNIV TRONDHEIM,TRONDHEIM,NORWAY

来源：

DIGESTIVE DISEASES AND SCIENCES | 1995年 / 40卷 / 08期

关键词：

GASTRIC MUCOSAL BLOOD FLOW; HYPEREMIC RESPONSE; MUCOSAL DAMAGE; PROSTAGLANDINS; HISTAMINE;

D O I：

10.1007/BF02212687

中图分类号：

R57 [消化系及腹部疾病];

学科分类号：

摘要：

This study was undertaken to examine the role of prostaglandins and histamine in the hyperemic response to gastric mucosal damage followed by H+ back-diffusion. Cat stomachs were exposed to 2 mol/liter NaCl for 10 min followed by luminal perfusion at pH 1. Hypertonic saline caused extensive (microscopic) damage to the surface epithelium, increased gastric mucosal blood flow, and increased release of histamine, PGE(2), and 6-keto PGF(1 alpha) (prostacyclin) into portal venous blood. The effect of indomethacin and histamine blockers (H-1 + H-2) on the hyperemic response to acid back-diffusion was related to the depth of the mucosal injury and the region of the stomach. In the corpus, indomethacin enhanced mucosal injury. In areas with superficial damage, the hyperemia was inhibited by indomethacin and antihistamines and eliminated by the combination of both. In corpus areas with indomethacin-induced deep lesions, the blood flow was very high, and this hyperemia was partly inhibited by antihistamines. In the antrum the hyperemic response was reduced by antihistamines. Indomethacin increased the release of histamine into the portal venous blood (baseline recordings) and reduced basal gastric mucosal blood how.

引用

页码：1669 / 1678

页数：10

共 35 条

[1]

Svanes K., Gislason H., Guttu K., Herfjord J.K., Fevang J., Gronbech J.E., Role of blood flow in adaptive protection of the cat gastric mucosa, Gastroenterology, 100, pp. 1249-1258, (1991)

[2]

Livingston E.H., Guth P.H., Antisecretory and cytoprotective doses of enprostil do not alter gastric mucosal blood flow, Life Sci, 52, pp. 1621-1628, (1993)

[3]

Leung F.W., Robert A., Guth P.H., Gastric mucosal blood flow in rats after administration of 16,16-dimethyl prostaglandin E<sub>2</sub> at a cytoprotective dose, Gastroenterology, 88, pp. 1948-1953, (1985)

[4]

Whittle B.J.R., Vane J.R., Prostanoids as regulators of gastrointestinal function, Physiology of the Gastrointestinal Tract, pp. 143-180, (1987)

[5]

Holzer P., Guth P.H., Neuropeptide control of rat gastric mucosal blood flow. Increase by calcitonin generalated peptide and vasoactive intestinal polypeptide, but not substance P and neurokinin A, Circ Res, 68, pp. 100-105, (1991)

[6]

Li D.S., Raybould H.E., Quintero E., Guth P.H., Calcitonin generelated peptide mediates the gastric hyperemic response to acid back-diffusion, Gastroenterology, 102, pp. 1124-1128, (1992)

[7]

Whittle B.J.R., Lopez-Belmonte J., Moncada S., Regulation of gastric mucosal integrity by endogenous nitric oxide: Interactions with prostanoids and sensory neuropeptides in the rat, Br J Pharmacol, 99, pp. 607-611, (1990)

[8]

Wood J.G., Darnell M.P., Cheung L.Y., Adenosine is a mediator of ethanol-induced gastric vasodilation in dogs, Am J Physiol, 264, pp. G664-G670, (1993)

[9]

Gislason H., Guttu K., Sorbye H., Schifter S., Waldum H.L., Svanes K., Role of histamine and calcitonin gene-related peptide (CGRP) in the hyperemic response to hypertonic saline and H<sup>+</sup> back-diffusion in the gastric mucosa of cats, Scand J Gastroenterol, 30, pp. 300-310, (1994)

[10]

Endoh K., Kao J., Domek M.J., Leung F.W., Mechanism of gastric hyperemia induced by intragastric hypertonic saline in rats, Gastroenterology, 104, pp. 114-121, (1993)

← 1 2 3 4 →