Aulí Mariona, Fernández Ester
Department of Cell Biology, Physiology and Immunology, Veterinary Faculty, Universitat Autònoma de Barcelona (UAB), Spain.
Life Sci. 2007 Sep 15;81(14):1117-29. doi: 10.1016/j.lfs.2007.08.001. Epub 2007 Aug 10.
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 microM), N-nitro-l-arginine (L-NOARG, 1 mM) and apamin (1 microM) 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.
旋毛虫诱导的大鼠结肠炎会引起结肠环行肌自发运动模式的改变[Auli, M., Fernandez, E., 2005. 旋毛虫诱导的大鼠结肠炎模型中功能和形态学变化的特征。《消化系统疾病与科学》50(8), 1432 - 1443]。我们研究了炎症严重程度与下层环行肌收缩性改变之间的时间关系，以及非肾上腺素能非胆碱能（NANC）抑制途径在运动模式破坏中的作用。通过直肠内注射旋毛虫幼虫诱导结肠炎。在感染后（PI）第2 - 30天，在器官浴中用假感染和感染大鼠的结肠环行肌条体外测定对乙酰胆碱（ACh）、细胞外钾增加的反应以及河豚毒素（TTX，1 microM）、N - 硝基 - l - 精氨酸（L - NOARG，1 mM）和蜂毒明肽（1 microM）的作用。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。与假感染组相比，感染后所有天数对ACh和KCl的反应均降低。细胞内钙耗竭在炎症组织（感染后6 - 14天）中有更大的抑制作用。发现TTX、L - NOARG和蜂毒明肽对所有感染大鼠的自发收缩的作用发生了改变，即它们的作用是短暂且较弱的。炎症组织显示出较低的静息膜电位以及电刺激诱导的抑制性接头电位持续时间缩短。这些数据表明，直肠内旋毛虫感染诱导的结肠环行平滑肌收缩性降低是由于兴奋 - 收缩偶联受损、平滑肌细胞持续超极化以及NANC抑制性神经传递受损所致。
