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Day-course changes in defecation refllex after rectal anastomosis and repairing the defecation reflex by promoting regeneration of the reflex pathways in the enteric nervous system by local treatment of BDNF

直肠吻合术后排便反射的日程变化以及BDNF局部治疗促进肠神经系统反射通路再生修复排便反射

基本信息

批准号：
18591477
负责人：
FUJII Hisao
金额：
$ 1.72万
依托单位：
Nara Medical University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2006
资助国家：
日本
起止时间：
2006 至 2007
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-18591477/
关键词：
brain-derived neurotrophic factor centeric nervous system internal anal sphincter plasticity guinea pig

项目摘要

Moderate rectal distension elicits rectal (R-R) reflex contractions and simultaneous internal anal sphincter (R-IAS) reflex relaxations that together comprise the defecation reflex. Both reflexes are controlled by (1) pelvic nerves, (2) lumbar colonic nerves, and (3) enteric nervous system. The aim of the present study was to explore a novel approach to repairing the defecation reflex dysfunction using the plasticity of enteric nervous pathways. Experiments were performed in anesthetized guinea pigs with ethyl carbamate. The rectum 30 mm oral from anal verge was transected without damage to extrinsic nerves, and subsequent end-to-end one layer anastomosis was performed. Recovery of the defecation reflex and associated reflex pathways were evaluated. Eight weeks after sectioning of intrinsic reflex nerve pathways in the rectum, the defecation reflex recovered to the control level, accompanied with regeneration of reflex pathways. The 5-HT_4 receptor agonist, mosapride (0.5 and 1.0 mg/kg) significantly (P < 0.01) enhanced the recovered defecation reflex eight weeks after surgery. Two weeks after the local treatment with brain-derived neurotrophic factor (BDNF: 10^-6g/ml)at the rectal anastomotic site, the R-IAS reflex relaxations recovered and some bundles of fine nerve fibers were shown to interconnect the oral and anal ends of the myenteric plexus. These results suggested a possibility for repairing the anal dysfunction by promoting regeneration of the reflex pathways in the enteric nervous system with local application of BDNF.

中度直肠扩张引起直肠(R-R)反射收缩和同时的肛门内括约肌(R-IAS)反射松弛，两者共同构成排便反射。这两种反射都由(1)盆腔神经、(2)腰结肠神经和(3)肠神经系统控制。本研究的目的是探索一种利用肠神经通路的可塑性修复排便反射障碍的新方法。用氨基甲酸乙酯麻醉豚鼠进行实验。在不损伤外周神经的情况下，切断距肛缘30 mm的直肠，行端端一层吻合术。评估排便反射及相关反射通路的恢复情况。切断直肠内反射神经通路8周后，排便反射恢复至对照水平，并伴有反射通路再生。5-HT4受体激动剂莫沙必利(0.5和1.0 mg/kg)可显著增强术后8周大鼠的排便反射。在直肠吻合口局部应用脑源性神经营养因子(BDNF：10~6g/ml)2周后，R-IAS反射松弛恢复，肌间神经丛的口、肛端可见一些细小的神经纤维束相互连接。提示局部应用脑源性神经营养因子可能通过促进肠神经系统反射通路的再生来修复肛门功能障碍。