Borges Luciano F, Caldini Elia G, Battlhener Cláudia N, Garcia Sérgio B, Zucoloto Sérgio, Montes Gregório S, Taboga Sebastião R
Laboratory of Cell Biology, Department of Pathology, The University of São Paulo School of Medicine, São Paulo, Brazil.
Micron. 2008 Jun;39(4):397-404. doi: 10.1016/j.micron.2007.03.004. Epub 2007 Mar 19.
Absence of enteric neurons is associated with thickening of the intestinal muscularis externa in Chagas' disease. The thickening is due to hyperplasia and hypertrophy of the smooth muscle cells and increased extracellular matrix components. The influence of the nervous system on the structure of the smooth muscle cells and its associated matrix has been poorly investigated. An experimental model of denervation of the ileum in rats was performed by application of the surfactant agent benzalkonium chloride that selectively destroys the myenteric plexus. Three months later, ileal tissue samples were obtained and studied by histochemistry and transmission electron microsocopy. Sham operated rats were used as controls. The diameter of collagen fibrils was evaluated in electron micrographs. The histopathological analysis showed thickening of the muscular layer. The thin and weakly arranged collagen and reticulin fibers surrounding the smooth muscle cells, observed in control cases by Picrosirius polarization (PSP) stain method, corresponded to a population of loosely packed thin collagen fibrils of uniform diameters (mean=29.16 nm) at the ultrastructural level. In contrast, the thick and strongly birefringent fibers around the muscle cells, observed in the treated group, stained by PSP, corresponded to densely packed thicker fibrils with large variation in diameter (mean=39.41 nm). Comparison of the data demonstrated statistically significant difference between the groups suggesting that the replacement of loosely arranged reticulin fibers by fibrous tissue (with typical collagen fiber), may alter the biomechanical function resulting in impairment of muscular contraction.
在恰加斯病中,肠神经元缺失与肠道外肌层增厚有关。这种增厚是由于平滑肌细胞的增生和肥大以及细胞外基质成分增加所致。神经系统对平滑肌细胞及其相关基质结构的影响尚未得到充分研究。通过应用选择性破坏肌间神经丛的表面活性剂苯扎氯铵,建立了大鼠回肠去神经支配的实验模型。三个月后,获取回肠组织样本,通过组织化学和透射电子显微镜进行研究。假手术大鼠用作对照。在电子显微镜照片中评估胶原纤维的直径。组织病理学分析显示肌层增厚。在对照病例中,通过天狼星红偏振(PSP)染色法观察到,围绕平滑肌细胞的薄且排列稀疏的胶原和网状纤维,在超微结构水平上对应于一群直径均匀(平均 = 29.16 nm)的松散排列的细胶原纤维。相比之下,在治疗组中观察到,经PSP染色,肌肉细胞周围厚且强双折射的纤维,对应于紧密堆积的较粗纤维,直径变化较大(平均 = 39.41 nm)。数据比较表明两组之间存在统计学上的显著差异,这表明由纤维组织(典型的胶原纤维)取代排列松散的网状纤维可能会改变生物力学功能,导致肌肉收缩受损。