Neuronal anomalies and normal muscle morphology at the hypomotile ileocecocolonic region of patients affected by idiopathic chronic constipation

Neuronal anomalies and normal muscle morphology at the hypomotile ileocecocolonic region of patients affected by idiopathic chronic constipation
复制标题

DOI:
10.14670/hh-14.1119
复制
发表时间:
1999-10-01
影响因子:
2
通讯作者:
Lise, M
Lise, M
中科院分区:
生物学4区
文献类型:
--
作者:
Faussone-Pellegrini, MS;Infantino, A;Lise, M

文献摘要

被引文献

相似文献

患有特发性慢传输慢性便秘的患者具有延迟的结肠传输,这可能与传播性收缩的减少或丧失有关。生肌和/或神经机制已被牵连在这种功能障碍的病理生理学和神经元异常已被描述在升结肠,降结肠和乙状结肠。在健康受试者中调节盲肠充盈和排空的回盲结肠区域的形态和运动行为从未在此类疾病中进行过研究。因此,我们通过内窥镜检查确定这些连接区是否存在运动障碍,并且在盲结肠连接处未发现自发性或激发性闭塞性收缩。整个结肠的光镜和电镜检查显示,神经元,平滑肌细胞和Cajal间质细胞的功能明显正常,而免疫组化和定量分析表明,在交界区的神经元异常。这些异常包括低的总神经元密度和显着少数VIP免疫反应神经元在两个肠神经丛,显着少数NOS免疫反应神经元在肌间神经丛和显着更多的NOS免疫反应神经元在粘膜下神经丛。这些发现排除了肌病,并证明存在神经病变。特别是,回盲结肠区域存在少量产生VIP和NO的神经元,这表明VIP和NO的产生可能减少,这可能导致松弛受损和/或传播性收缩的开始,从而减慢药团输送。近端结肠存在这种异常可能解释了为什么左结肠切除术和/或盲肠直肠吻合术在这种疾病的患者中不成功。
Patients suffering from idiopathic slow-transit chronic constipation have a delayed colonic transit referable to a decrease or loss of propagating contractions. Myogenic and/or neural mechanisms have been implicated in the pathophysiology of this dysfunction and neuronal abnormalities have been described at the ascending, descending and sigmoid colon. The morphology and motile behaviour of the ileocecocolonic region, which in healthy subjects regulates cecum filling and emptying, have never been investigated in such disease. Therefore, we endoscopically ascertained whether a motility impairment was present at these junctional areas and neither spontaneous nor provoked occlusive contractions were found at the cecocolonic junction. Light and electron microscope examination of the entire colon revealed apparently normal features of neurons, smooth muscle cells and interstitial cells of Cajal, while immunohistochemistry and quantitative analysis demonstrated neuronal anomalies at the junctional areas. These anomalies consisted of low total neuron density and significantly few VIP-immunoreactive neurons at the two enteric plexuses, significantly few NOS-immunoreactive neurons at the myenteric plexus and significantly more NOS-immunoreactive neurons at the submucous plexus. These findings exclude a myopathy and demonstrate the existence of a neuropathy. In particular, the presence at the ileocecocolonic region of few VIP- and NO-producing neurons suggests that there might be a reduced VIP and NO production which may result in a compromised relaxation and/or onset of propagating contractions, slowing down bolus transit. The presence at the proximal colon of such an abnormality might explain why left colectomy and/or cecorectal anastomosis are unsuccessful in patients with this disease.