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2
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3
Topical nicotine protects rat gastric mucosa against ASA-induced damage. A role for mucosal fluid secretion in cytoprotection.局部应用尼古丁可保护大鼠胃黏膜免受阿司匹林诱导的损伤。黏膜液分泌在细胞保护中的作用。
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本文引用的文献

1
A rapid, quantitative GLC method for the simultaneous determination of nicotine and cotinine.一种同时测定尼古丁和可替宁的快速定量气相色谱法。
J Anal Toxicol. 1982 Nov-Dec;6(6):294-6. doi: 10.1093/jat/6.6.294.
2
Regional gastric mucosal blood flow measurements by hydrogen gas clearance in the anesthetized rat and rabbit.通过氢气清除法测量麻醉大鼠和家兔的局部胃黏膜血流量。
Gastroenterology. 1984 Jul;87(1):28-36.
3
Assay of nicotine in biological materials: sources of contamination and their elimination.生物材料中尼古丁的检测:污染来源及其消除
J Pharm Pharmacol. 1980 Mar;32(3):178-81. doi: 10.1111/j.2042-7158.1980.tb12885.x.
4
Parenteral aspirin and sodium salicylate are equally injurious to the rat gastric mucosa.肠胃外给予的阿司匹林和水杨酸钠对大鼠胃黏膜的损伤程度相同。
Gastroenterology. 1987 Oct;93(4):863-71. doi: 10.1016/0016-5085(87)90451-3.
5
Effect of aspirin plus hydrochloric acid on the gastric mucosal microcirculation.阿司匹林加盐酸对胃黏膜微循环的影响。
Gastroenterology. 1987 Oct;93(4):810-7. doi: 10.1016/0016-5085(87)90444-6.
6
Effects of non-steroidal anti-inflammatory drugs on rat gastric mucosal leukotriene C4 and prostanoid release: relation to ethanol-induced injury.非甾体抗炎药对大鼠胃黏膜白三烯C4和类前列腺素释放的影响:与乙醇诱导损伤的关系。
Br J Pharmacol. 1988 Apr;93(4):937-43. doi: 10.1111/j.1476-5381.1988.tb11483.x.
7
Vascular injury in acute gastric mucosal damage. Mediatory role of leukotrienes.急性胃黏膜损伤中的血管损伤。白三烯的介导作用。
Dig Dis Sci. 1988 May;33(5):625-32. doi: 10.1007/BF01798368.
8
Failure of the inhibition of rat gastric mucosal 5-lipoxygenase by novel acetohydroxamic acids to prevent ethanol-induced damage.新型乙酰氧肟酸对大鼠胃黏膜5-脂氧合酶抑制作用未能预防乙醇诱导的损伤。
Br J Pharmacol. 1988 Sep;95(1):155-62. doi: 10.1111/j.1476-5381.1988.tb16559.x.
9
Gastric vasoconstrictor actions of leukotriene C4, PGF2 alpha, and thromboxane mimetic U-46619 on rat submucosal microcirculation in vivo.白三烯C4、前列腺素F2α及血栓素类似物U-46619对大鼠体内胃黏膜下微循环的缩血管作用。
Am J Physiol. 1985 May;248(5 Pt 1):G580-6. doi: 10.1152/ajpgi.1985.248.5.G580.
10
Effects of ethanol and nicotine on gastrin and somatostatin release in rats.乙醇和尼古丁对大鼠胃泌素和生长抑素释放的影响。
Horm Res. 1987;25(2):113-9. doi: 10.1159/000180641.

长期摄入尼古丁会导致大鼠胃黏膜血管调节功能紊乱。

Chronic nicotine intake causes vascular dysregulation in the rat gastric mucosa.

作者信息

Battistel M, Plebani M, Di Mario F, Jocic M, Lippe I T, Holzer P

机构信息

University of Graz, Department of Experimental and Clinical Pharmacology, Austria.

出版信息

Gut. 1993 Dec;34(12):1688-92. doi: 10.1136/gut.34.12.1688.

DOI:10.1136/gut.34.12.1688
PMID:8282257
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1374464/
Abstract

Chronic cigarette smoking has adverse effects on peptic ulcer disease because the healing of ulcers is delayed and the incidence of relapses is enhanced. Short term intake of nicotine induces vascular damage in the rat gastric mucosa, but the pathophysiological mechanisms of nicotine's action in the stomach are largely unknown. In this study rats were treated with nicotine, added to their drinking water, for 50 days. They were then anaesthetised and their stomachs perfused with acidified acetylsalicylic acid (ASA). Chronic nicotine treatment failed to change the effects of acidified ASA to induce gastric mucosal acid back diffusion, haemorrhagic damage and bleeding. Basal blood flow in the gastric mucosa was also unchanged by chronic nicotine intake, whereas the mucosal hyperaemia evoked by ASA induced acid back diffusion was averted. The concentrations of sulfidoleukotrienes were significantly augmented in the gastric wall of nicotine treated rats. These data show that chronic nicotine intake causes dysregulation of the gastric microcirculation, an effect that is associated with biochemical changes in the stomach. This study thus substantiates the adverse effects of smoking on gastric mucosal pathophysiology. These data suggest that inappropriate regulation of gastric mucosal blood flow inhibits recovery from gastric mucosal injury in smokers.

摘要

长期吸烟对消化性溃疡病有不良影响,因为溃疡愈合延迟且复发率增加。短期摄入尼古丁会导致大鼠胃黏膜血管损伤,但尼古丁在胃中的作用的病理生理机制很大程度上尚不清楚。在本研究中,给大鼠饮用添加了尼古丁的水,持续50天。然后将它们麻醉,并用酸化的乙酰水杨酸(ASA)灌注其胃部。长期尼古丁治疗未能改变酸化ASA诱导胃黏膜酸反向弥散、出血性损伤和出血的作用。长期摄入尼古丁也未改变胃黏膜的基础血流量,而由ASA诱导的酸反向弥散引起的黏膜充血则得以避免。在尼古丁处理的大鼠胃壁中,硫代白三烯的浓度显著增加。这些数据表明,长期摄入尼古丁会导致胃微循环失调,这种效应与胃中的生化变化有关。因此,本研究证实了吸烟对胃黏膜病理生理学的不良影响。这些数据表明,胃黏膜血流调节不当会抑制吸烟者胃黏膜损伤的恢复。