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Familial megacecum and colon in the rat: a new model of gastrointestinal neuromuscular dysfunction

机译：大鼠家族性大盲肠和结肠：胃肠道神经肌肉功能障碍的新模型

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摘要

Gastrointestinal motility disorders are of considerable clinical importance in humans and animals. Abnormalities of smooth muscle and the enteric nervous system have been described. We have identified and characterized a new mutant stock of rats that develops severe megacecum and colon with pseudo-obstruction, Familial Megacecum and Colon (FMC). The inheritance pattern of FMC was characterized by selective breeding. Gastrointestinal motility was evaluated radiographically. Complete pathologic evaluations, including ultrastructural examination and staining of colonic segments for acetylcholinesterase, peripherin, vasoactive intestinal peptide, substance P, nitric oxide synthase, and somatostatin, were performed. Spontaneous contractility and contractile force in isolated colonic muscle strips were examined. Familial megacecum and colon is inherited as an autosomal recessive trait. The markedly dilated cecum and proximal portion of the colon are followed by a short, funnel-shaped segment and distal portion of the colon with normal or slightly reduced lumen. Although clinical features and gross anatomic changes of the colon resemble those of Hirschsprung's disease in humans and animals, aganglionosis is not a feature of FMC. An increase in somatostatin staining was observed in dilated regions of bowel. The spontaneous contractile frequency and contractile force were diminished in the affected colon. Familial megacecum and colon is a new mutant, distinct from previously described hereditary and targeted mutant rodent models that develop megacecum and colon as a result of distal colonic dysfunction. The functional or morphologic defect(s) that result in colonic dysfunction in rats with FMC was not determined. The disease may result from an absence or overexpression of a single or group of neurotransmitters or their respective neurons, receptor abnormalities, or defects in the intestinal pacemaker system.
机译：胃肠动力障碍在人类和动物中具有重要的临床意义。已经描述了平滑肌和肠神经系统的异常。我们已经鉴定并鉴定了新的大鼠突变体种群，该种群发展出严重的大盲肠和结肠，并伴有假性梗阻，家族性大盲肠和结肠（FMC）。 FMC的遗传模式以选择性育种为特征。影像学评估胃肠蠕动。进行了完整的病理学评估，包括超微结构检查和结肠节段的乙酰胆碱酯酶，外周血蛋白，血管活性肠肽，P物质，一氧化氮合酶和生长抑素染色。检查孤立的结肠肌条中的自发收缩力和收缩力。家族性大盲肠和结肠作为常染色体隐性遗传。盲肠和结肠近端部分明显扩张，其后是短而漏斗形的部分和结肠远端，管腔正常或略微缩小。尽管在人和动物中结肠的临床特征和总体解剖学变化类似于赫希斯氏病，但神经节病不是FMC的特征。在肠的扩张区域中观察到生长抑素染色的增加。受累结肠的自发收缩频率和收缩力降低。家族性大盲肠和结肠是一种新的突变体，不同于先前描述的由于远端结肠功能障碍而导致的大盲肠和结肠的遗传性和靶向性突变啮齿动物模型。尚未确定导致FMC大鼠结肠功能障碍的功能或形态缺陷。该疾病可能是由于单个或一组神经递质或它们各自的神经元的缺乏或过表达，肠道异常或肠道起搏器系统缺陷引起的。

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