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先天性巨结肠症中神经节性和无神经节性结肠胆碱能神经效应器传递的特征

Characteristics of cholinergic neuroeffector transmission of ganglionic and aganglionic colon in Hirschsprung's disease.

作者信息

Vizi E S, Zséli J, Kontor E, Feher E, Verebélyi T

机构信息

Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest.

出版信息

Gut. 1990 Sep;31(9):1046-50. doi: 10.1136/gut.31.9.1046.

DOI:10.1136/gut.31.9.1046
PMID:2170248
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1378667/
Abstract

Differences in the release and content of acetylcholine and the alpha 2 adrenoceptor mediated interaction between noradrenergic and cholinergic neurons were investigated by neurochemical and pharmacological methods in aganglionic and ganglionic segments of isolated human colon taken from children suffering from Hirschsprung's disease. Both at rest and during transmural stimulation the release of acetylcholine was significantly higher in the spastic (aganglionic) segment than in the proximal dilated bowel. Significant differences were found in the tissue concentration of acetylcholine between ganglionic and aganglionic specimens. The pattern of response to transmural stimulation was also different in the spastic and dilated bowel. Transmural stimulation induced relaxation and contraction in ganglionic specimens but only contractions in aganglionic specimens. The sensitivity of the smooth muscle in the aganglionic portion to exogenous acetylcholine and to field stimulation was found to be higher than in the ganglionic portion. While noradrenaline added to the organ bath reduced the stimulation-evoked release of acetylcholine from spastic segments, via an alpha 2 adrenoceptor mediated process, yohimbine did not enhance the release. It is suggested that in Hirschsprung's disease the increased acetylcholine release, the enhanced sensitivity of smooth muscle cells to acetylcholine, and the lack of alpha 2 adrenoceptor mediated noradrenergic modulation of acetylcholine release from cholinergic interneurons might be responsible for the spasm of aganglionic segments.

摘要

采用神经化学和药理学方法,对取自患有先天性巨结肠症儿童的离体人结肠无神经节段和有神经节段进行研究,以探讨乙酰胆碱释放及含量的差异,以及去甲肾上腺素能神经元与胆碱能神经元之间由α2肾上腺素能受体介导的相互作用。无论是在静息状态还是在跨壁刺激期间,痉挛(无神经节)段中乙酰胆碱的释放均显著高于近端扩张肠段。有神经节标本和无神经节标本之间,乙酰胆碱的组织浓度存在显著差异。痉挛肠段和扩张肠段对跨壁刺激的反应模式也有所不同。跨壁刺激在有神经节标本中引起舒张和收缩,但在无神经节标本中仅引起收缩。发现无神经节部分平滑肌对外源性乙酰胆碱和场刺激的敏感性高于有神经节部分。虽然添加到器官浴中的去甲肾上腺素通过α2肾上腺素能受体介导的过程减少了痉挛段中刺激诱发的乙酰胆碱释放,但育亨宾并未增强这种释放。提示在先天性巨结肠症中,乙酰胆碱释放增加、平滑肌细胞对乙酰胆碱的敏感性增强以及胆碱能中间神经元释放的乙酰胆碱缺乏α2肾上腺素能受体介导的去甲肾上腺素能调节,可能是无神经节段痉挛的原因。

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