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肠神经系统在肠外营养中的分析。

Colonic enteric nervous system analysis during parenteral nutrition.

机构信息

Department of Neuroscience, University of Wisconsin-Madison School of Medicine and Public Health, Madison, Wisconsin 53792, USA.

出版信息

J Surg Res. 2013 Sep;184(1):132-7. doi: 10.1016/j.jss.2013.02.044. Epub 2013 Mar 16.

DOI:10.1016/j.jss.2013.02.044
PMID:23601532
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3947919/
Abstract

INTRODUCTION

Parenteral nutrition (PN) is a necessary therapy used to feed patients with gastrointestinal dysfunction. Unfortunately, PN results in intestinal atrophy and changes to host immune function. PN may also induce additional effects on gut motility that we hypothesized would result from changes in the enteric nervous system.

METHODS

Mice received an intravenous (i.v.) catheter and were randomized to chow (n = 5), i.v. PN (n = 6), or i.v. PN + bombesin (BBS, 15 μg/kg, 3×/d) (n = 6) for 5 d. Colons were removed and dissected to measure the length and circumference. Enteric neuronal density and neurotransmitter expression were determined by co-immunostaining whole-mount tissue with Hu and neuronal nitric oxide synthase (nNOS).

RESULTS

The number of myenteric neurons expressing Hu and nNOS increased per unit length in the mid-colon during PN treatment compared with chow. This increase was abrogated by the addition of BBS to the PN regimen. However, the percentage of nNOS-expressing neurons was not significantly altered by PN. Morphometric analysis revealed a decrease in the length and circumference of the colon during PN administration that was partially normalized by supplementation of PN with BBS. A significant reduction in total fecal output was observed in PN animals compared with chow and was increased by mice receiving BBS in addition to PN.

CONCLUSIONS

PN causes a constriction of the bowel wall, reducing not only the length but also the circumference of the colon. These changes cause a condensation of enteric neurons but no difference in neurotransmitter expression. BBS supplementation partially restores the constriction and increases the fecal output during PN treatment compared with PN treatment alone.

摘要

简介

肠外营养(PN)是一种用于喂养胃肠道功能障碍患者的必要治疗方法。不幸的是,PN 会导致肠萎缩和宿主免疫功能改变。PN 还可能对肠道蠕动产生其他影响,我们假设这些影响是由于肠神经系统的变化引起的。

方法

小鼠接受静脉(i.v.)导管,并随机分为正常饮食(n = 5)、静脉 PN(n = 6)或静脉 PN + 蛙皮素(BBS,15μg/kg,3×/d)(n = 6)治疗 5 天。取出结肠并解剖以测量长度和周长。通过用 Hu 和神经元型一氧化氮合酶(nNOS)对整个组织进行共免疫染色来确定肠神经元密度和神经递质表达。

结果

与正常饮食相比,PN 治疗期间中结肠的 Hu 和 nNOS 表达神经元数量每单位长度增加。BBS 添加到 PN 方案中可消除这种增加。然而,PN 对 nNOS 表达神经元的百分比没有显著影响。形态计量学分析显示,PN 给药期间结肠的长度和周长减少,BBS 补充 PN 可部分恢复正常。与正常饮食和接受 BBS 加 PN 的小鼠相比,PN 动物的总粪便排出量明显减少。

结论

PN 导致肠壁收缩,不仅减少了结肠的长度,而且减少了其周长。这些变化导致肠神经元的凝聚,但神经递质表达没有差异。与单独 PN 治疗相比,BBS 补充部分恢复了 PN 治疗期间的收缩并增加了粪便排出量。

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