Ribeiro U, Safatle-Ribeiro A V, Habr-Gama A, Gama-Rodrigues J J, Sohn J, Reynolds J C
Department of Surgery, University of Pittsburgh, Pennsylvania, USA.
Dis Colon Rectum. 1998 Nov;41(11):1411-7. doi: 10.1007/BF02237058.
The pathophysiology of Chagas' disease is incompletely understood. Neuronal nitric oxide has been cited as a candidate neurotransmitter responsible for relaxation of the internal anal sphincter. Neuronal nicotinamide adenine dinucleotide phosphate diaphorase can be used as a marker for neuronal nitric oxide synthase. This study was designed to examine the alterations of the nitric oxide-containing neurons in the enteric nervous system of the colon of patients who underwent resections for advanced megacolon and to compare these specimens with small-bowel specimens from the same patients and with specimens from control subjects.
Specimens from resected rectum and extramucosal small-bowel biopsy specimens from 11 patients with Chagas megacolon but no apparent small-bowel clinical involvement were compared with the uninvolved colon and jejunum of 10 control patients with colon cancer. Tissues were fixed in Zamboni solution and evaluated by histochemistry for nicotinamide adenine dinucleotide phosphate diaphorase-containing neurons. Reactivity was evaluated on a 0 to 4 scale in the longitudinal muscle, myenteric plexus, circular muscle, submucosal plexus, and mucosa.
Specimens from control patients showed well-stained myenteric and submucosal neurons and an abundant network of terminal nerve fibers in the muscle layers. Chagasic specimens had decreased staining in all layers of the gut. Overall there was a statistically significant decrease in nicotinamide adenine dinucleotide phosphate diaphorase-containing neurons. Biopsy specimens from clinically uninvolved small bowel of patients with Chagas' disease also showed decreased reactivity, but to a lesser degree.
Nicotinamide adenine dinucleotide phosphate diaphorase activity is decreased in patients with advanced megacolon. The alterations are more relevant in the myenteric plexus and the circular muscle. Reactivity is also diminished in the clinically uninvolved small bowel, but to a lesser extent.
恰加斯病的病理生理学尚未完全明了。神经元型一氧化氮被认为是负责肛门内括约肌松弛的候选神经递质。神经元型烟酰胺腺嘌呤二核苷酸磷酸黄递酶可作为神经元型一氧化氮合酶的标志物。本研究旨在检查因晚期巨结肠接受切除术患者结肠的肠神经系统中含一氧化氮神经元的变化，并将这些标本与同一患者的小肠标本以及对照受试者的标本进行比较。
将11例患有恰加斯巨结肠但无明显小肠临床受累的患者的切除直肠标本和黏膜外小肠活检标本，与10例患有结肠癌的对照患者的未受累结肠和空肠进行比较。组织用赞博尼溶液固定，并通过组织化学评估含烟酰胺腺嘌呤二核苷酸磷酸黄递酶的神经元。在纵肌、肌间神经丛、环肌、黏膜下神经丛和黏膜中，以0至4级评估反应性。
对照患者的标本显示肌间和黏膜下神经元染色良好，肌层有丰富的终末神经纤维网络。恰加斯病患者的标本在肠道各层的染色均减少。总体而言，含烟酰胺腺嘌呤二核苷酸磷酸黄递酶的神经元在统计学上有显著减少。恰加斯病患者临床未受累小肠的活检标本反应性也降低，但程度较轻。
晚期巨结肠患者烟酰胺腺嘌呤二核苷酸磷酸黄递酶活性降低。这些变化在肌间神经丛和环肌中更为明显。临床未受累小肠的反应性也降低，但程度较小。
