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兔空肠中黏蛋白和蛋白质的释放:氨甲酰甲胆碱和迷走神经刺激的作用。

Mucin and protein release in the rabbit jejunum: effects of bethanechol and vagal nerve stimulation.

作者信息

Greenwood B, Mantle M

机构信息

Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee.

出版信息

Gastroenterology. 1992 Aug;103(2):496-505. doi: 10.1016/0016-5085(92)90839-q.

Abstract

The role of the vagus nerve and cholinergic mechanisms in the control of rabbit jejunal mucin and protein release was investigated in vivo. In anesthetized animals, a 10-cm segment of the jejunum was cannulated and perfused with saline. Perfusate was collected and analyzed for mucin (by immunoassay) and protein. Bilateral cervical vagotomy had no effect on basal mucin or protein output, suggesting that the vagus nerve does not exert a tonic control on jejunal macromolecule secretion. Electrical stimulation of the vagi did not alter mucin release, even in the presence of muscarinic cholinergic (scopolamine) or adrenergic (propranolol and phentolamine) blockade. In contrast, protein output increased significantly after vagal stimulation, an effect inhibited by scopolamine. In both vagotomized and vagally intact rabbits, the cholinergic agonist bethanechol (200 micrograms/kg intraperitoneally) induced a scopolamine-sensitive increase in both mucin and protein output. Predominantly serum proteins were released into intestinal perfusates after vagal or cholinergic stimulation. It is concluded that the extrinsic vagus nerve does not regulate rabbit jejunal mucin secretion in vivo and that cholinergic control of intestinal goblet cells is implemented entirely by the intrinsic enteric nervous system. In addition, cholinergic or vagal stimulation increases intestinal vascular and epithelial permeability, resulting in the passage of serum proteins into the lumen, possibly by opening tight junctions and paracellular pathways.

摘要

在体内研究了迷走神经和胆碱能机制在控制兔空肠粘蛋白和蛋白质释放中的作用。在麻醉动物中,将空肠的一段10厘米长的肠段插管并用生理盐水灌注。收集灌注液并分析其中的粘蛋白(通过免疫测定法)和蛋白质。双侧颈迷走神经切断术对基础粘蛋白或蛋白质输出没有影响,这表明迷走神经对空肠大分子分泌没有紧张性控制作用。即使存在毒蕈碱胆碱能(东莨菪碱)或肾上腺素能(普萘洛尔和酚妥拉明)阻断,迷走神经的电刺激也不会改变粘蛋白的释放。相反,迷走神经刺激后蛋白质输出显著增加,这种作用被东莨菪碱抑制。在迷走神经切断和迷走神经完整的兔子中,胆碱能激动剂氨甲酰甲胆碱(200微克/千克腹腔注射)均可引起粘蛋白和蛋白质输出的东莨菪碱敏感型增加。迷走神经或胆碱能刺激后,主要是血清蛋白释放到肠道灌注液中。得出的结论是,外在迷走神经在体内不调节兔空肠粘蛋白分泌,并且肠道杯状细胞的胆碱能控制完全由内在的肠神经系统实现。此外,胆碱能或迷走神经刺激会增加肠道血管和上皮的通透性,可能通过打开紧密连接和细胞旁途径,导致血清蛋白进入肠腔。

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