Jacobson K, McHugh K, Collins S M
Department of Medicine, McMaster University Medical Center, Hamilton, Ontario, Canada.
Gastroenterology. 1995 Sep;109(3):718-22. doi: 10.1016/0016-5085(95)90378-x.
BACKGROUND & AIMS: Studies in inflammatory bowel disease have shown extensive structural abnormalities in the enteric nervous system of inflamed and noninflamed gut; however, functional correlates are lacking. The aim of this study was to determine the effect of colitis on myenteric nerve function at inflamed and noninflamed sites in rat intestine.
Tritiated noradrenaline release was measured from longitudinal muscle myenteric plexus preparations from the distal and transverse colon and terminal ileum of rats with colitis induced by trinitrobenzene sulfonic acid or Trichinella spiralis larvae.
As characterized by myeloperoxidase activity and histology, both models induced inflammation restricted to the distal colon. In distal colon in trinitrobenzene sulfonic acid colitis, KCl- or electrical field stimulation-evoked 3H release was suppressed by 56% and 60%, respectively; in T. spiralis-infected rats, the KCl-evoked release was suppressed by 58%. 3H release was also suppressed by similar magnitudes in noninflamed transverse colon and terminal ileum of each model.
Experimental distal colitis alters myenteric nerve function in inflamed distal colon and noninflamed gut regions. These changes are independent of the manner in which colitis is induced and provide a basis for the extensive disruption of physiological function observed in inflammatory bowel disease.
炎症性肠病的研究表明，炎症肠道和非炎症肠道的肠神经系统均存在广泛的结构异常；然而，缺乏功能相关性研究。本研究旨在确定结肠炎对大鼠肠道炎症部位和非炎症部位肌间神经功能的影响。
测量用三硝基苯磺酸或旋毛虫幼虫诱导结肠炎的大鼠远端结肠、横结肠和回肠末端纵行肌肌间神经丛标本中氚标记去甲肾上腺素的释放量。
以髓过氧化物酶活性和组织学特征为依据，两种模型均诱导了局限于远端结肠的炎症。在三硝基苯磺酸结肠炎模型的远端结肠，氯化钾或电场刺激诱发的3H释放分别被抑制了56%和60%；在旋毛虫感染的大鼠中，氯化钾诱发的释放被抑制了58%。在每个模型的非炎症横结肠和回肠末端，3H释放也被抑制了相似程度。
实验性远端结肠炎改变了炎症远端结肠和非炎症肠道区域的肌间神经功能。这些变化与结肠炎的诱导方式无关，并为炎症性肠病中观察到的生理功能广泛紊乱提供了依据。
