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香烟烟雾诱导大鼠十二指肠黏膜碳酸氢盐分泌的神经激素机制

Neurohormonal mechanisms of cigarette smoke-induced duodenal mucosal bicarbonate secretion in the rat.

作者信息

Murthy S, Dinoso V P, Natrajan R

机构信息

Division of Gastroenterology and Hepatology, Allegheny University of the Health Sciences University, Philadelphia, PA 19102-1192, USA.

出版信息

Peptides. 1997;18(7):1061-6. doi: 10.1016/s0196-9781(97)00030-2.

DOI:10.1016/s0196-9781(97)00030-2
PMID:9357067
Abstract

The effect of cigarette smoke and nicotine on duodenal mucosal bicarbonate secretion (DMBS) was studied in rats. Cigarette smoke but not intravenous nicotine administered acutely to anesthetized rats via a tracheostomy tube stimulated DMBS by 47 +/- 6%. The increase was neurally mediated via atropine-sensitive postganglionic cholinergic neurons. Introduction of cigarette smoke after the infusion of vasoactive intestinal peptide and porcine histidine isoleucine (PHI) also caused a delayed increase in DMBS. However, the magnitude of this increase was similar to that seen in control non-peptide-infused rats. The increase in bicarbonate secretion predominantly involved Brunner's glands. Rats exposed to cigarette smoke for 4 and 8 days before direct instillation of smoke via tracheostomy tube did not show any increase in their DMBS. These studies indicate that in the rat, cigarette smoke increases DMBS, most likely secreted by the Brunner's glands. The increase is neurally mediated via atropine-sensitive postganglionic cholinergic neurons. Gastroenteric neuropeptides do not exert any influence on cigarette smoke-mediated DMBS secretion in the rat. Unlike acute exposure to cigarette smoke, chronic exposure (4 and 8 days) of rats to cigarette smoke abolishes increase in DMBS induced by subsequent exposure to cigarette smoke. This last observation may, in part, may explain the tendency of chronic smokers who have duodenal bulb ulcers to show greater propensity to higher rate of recurrence and protracted healing.

摘要

研究了香烟烟雾和尼古丁对大鼠十二指肠黏膜碳酸氢盐分泌(DMBS)的影响。通过气管造口管对麻醉大鼠急性给予香烟烟雾而非静脉注射尼古丁,可使DMBS增加47±6%。这种增加是通过对阿托品敏感的节后胆碱能神经元经神经介导的。在输注血管活性肠肽和猪组氨酸异亮氨酸(PHI)后引入香烟烟雾,也会导致DMBS延迟增加。然而,这种增加的幅度与未输注肽的对照大鼠相似。碳酸氢盐分泌的增加主要涉及Brunner腺。在通过气管造口管直接滴入烟雾前4天和8天暴露于香烟烟雾的大鼠,其DMBS没有任何增加。这些研究表明,在大鼠中,香烟烟雾会增加DMBS,很可能是由Brunner腺分泌的。这种增加是通过对阿托品敏感的节后胆碱能神经元经神经介导的。胃肠神经肽对大鼠香烟烟雾介导的DMBS分泌没有任何影响。与急性暴露于香烟烟雾不同,大鼠慢性暴露(4天和8天)于香烟烟雾会消除随后暴露于香烟烟雾所诱导的DMBS增加。这最后一个观察结果可能部分解释了患有十二指肠球部溃疡的慢性吸烟者显示出更高复发率和愈合延迟倾向的原因。

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