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作 者:席红卫[1] 吴晓霞[1] 崔彦北[1] 王建峰[1]
出 处:《中华小儿外科杂志》2008年第5期281-283,共3页Chinese Journal of Pediatric Surgery
摘 要:目的了解梅克尔憩室(MD)肠壁神经和平滑肌病理组织学改变,探讨MD及其并发症的发病机制。方法收集2004年1月至2006年7月手术切除的44例MD标本,另取6例死于与肠道和神经系统无关疾病的足月新生儿尸检小肠标本为对照,采用常规HE染色计数肠壁肌间神经丛和丛内神经节细胞数,8-100蛋白、神经元特异性烯醇化酶(NSE)和平滑肌肌动蛋白(α-SMA)采用免疫组织化学染色(SABC法)。结果MD的肠壁肌间神经丛密度与对照组相比无统计学意义(P〉0.05),但丛内神经节细胞数、单个肌间神经丛的平均面积及其平均神经丛长轴长度均较对照组减少,而平均光密度值比对照组增加。肌间神经丛的平均面积与其平均吸光度呈负相关(r=-0.215,P〈0.05),且上述病理改变以症状组和伴有异位胃黏膜的MD尤为突出。MD的肠壁环肌层和纵肌层旷SMA表达减低,环肌层肥厚;而距憩室5cm处肠壁肌间神经丛的各项指标的改变均减轻,但是环肌层仍明显肥厚,α-SMA染色亦减轻。结论肠壁神经丛和平滑肌细胞的变化可能参与了MD及其并发症的发生。Objective To investigate the pathologic changes of enteric nerves and smooth muscle cells of Meckel's diverticulum, and its relationship to the complications. Methods Full thickness samples were obtained from 44 patients during operation on Meckel's diverticulitis between January 2004 and July 2006. The intestines from newborns that died from causes unrelated to gastrointestinal or nervous system diseases were selected as controls. All specimens were stained with haematoxylin and eosin (HE) and SABC immunohistochemistry. Results There was no significant difference in the density of mesenteric nerve plexus between the two groups (P〉0. 05). The reduction of ganglionic cells and average long axis of mesenteric nerve plexus with an increasing of mean optical density were observed on Meckel's diverticulitis. There were negative correlation of the average area of mesenteric plexus with the mean optical absorbance ( r= - 0. 215,P〈0. 05) ,which was obvious in specimens of diverticulitis with ectopic gastric mucosa. A remarkable decrease in staining intensity of α-SMA was mainly observed on the hypertrophic circular muscular layer of Meckel's diverticulitis. The alteration patterns of mesenteric ganglionic plexus were markedly reduced at intestine more than 5 cm apart from the (diverticulum, but the circular muscle was still hypertrophy with a decrease inα-SMA expression. Conclusions The authors consider that the alternations of enteric nerves and smooth muscles might contribute to the pathogenesis of Meckel's diverticulitis.
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