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Time course of neural and contractile disturbances in a rat model of colitis induced by Trichinella spiralis

机译：旋毛虫诱发的结肠炎大鼠模型中神经和收缩障碍的时程

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Colitis induced by Trichinella spiralis in rat induces alterations in the spontaneous motor pattern displayed by circular colonic muscle [Auli, M., Fernandez, E., 2005. Characterization of functional and morphological changes in a rat model of colitis induced by T. spiralis. Digestive Diseases and Sciences 50(8), 1432-1443]. We examined the temporal relationship between the severity of inflammation and the altered contractility of the underlying circular muscle as well as the role of NANC inhibitory pathways in the disruption of the motility pattern. Colitis was induced by intrarectal administration of T. spiralis larvae. Responses to acetylcholine (ACh) and increased extracellular potassium as well as the effect of tetrodotoxin (TTX, 1 mu M), N-nitro-L-arginine (L-NOARG, 1 mM) and apamin (1 mu M) were determined in vitro in the organ bath with circular muscle strips from sham-infected and infected rats at days 2-30 postinfection (PI). Microelectrode recordings were performed to study the putative changes in electrical activity of colonic smooth muscle cells. Responses to ACh and KCl were decreased at all days PI compared to sham. Intracellular calcium depletion had a greater inhibitory effect in inflamed tissue (6-14 PI). The effect of TTX, L-NOARG and apamin on the spontaneous contractions was found to be altered in all infected rats, i.e. their effects were transient and milder. Inflamed tissue showed lower resting membrane potential and a decreased duration of inhibitory junction potentials induced by electrical stimulation. These data suggest that the decreased contractility of colonic circular smooth muscle induced by the intrarectal T. spiralis infection results from the impairment of the excitation-contraction coupling, from a persistent hyperpolarization of smooth muscle cells and from impaired NANC inhibitory neurotransmission. (C) 2007 Elsevier Inc. All rights reserved.
机译：由旋毛虫在大鼠中诱发的结肠炎诱导了由结肠结肠肌表现出的自发运动模式的改变[Auli，M.，Fernandez，E.，2005。在由T.spiralis诱发的大鼠结肠炎模型中功能和形态变化的表征。消化系统疾病50（8），1432-1443]。我们检查了炎症严重程度与基础环形肌肉收缩力改变之间的时间关系，以及NANC抑制途径在运动模式破坏中的作用。结肠炎是通过直肠内施用螺旋螺旋体幼虫引起的。测定了对乙酰胆碱（ACh）和细胞外钾增加的反应以及河豚毒素（TTX，1μM），N-硝基-L-精氨酸（L-NOARG，1 mM）和阿帕明（1μM）的影响。在感染后第2-30天，在器官浴中用深部感染和感染的大鼠的环形肌条进行体外培养。进行微电极记录以研究结肠平滑肌细胞电活动的假定变化。与假手术相比，PI在所有天中对ACh和KCl的反应均降低。细胞内钙耗竭对发炎的组织具有更大的抑制作用（6-14 PI）。发现在所有感染的大鼠中，TTX，L-NOARG和木瓜蛋白酶对自发性收缩的作用均发生了改变，即它们的作用是短暂且较温和的。发炎的组织显示出较低的静息膜电位和电刺激诱导的抑制性连接电位持续时间减少。这些数据表明，由直肠内螺旋螺旋体感染引起的结肠环形平滑肌收缩力的降低是由于兴奋收缩耦合受损，平滑肌细胞持续超极化以及NANC抑制性神经传递受损引起的。 （C）2007 Elsevier Inc.保留所有权利。

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