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肛门直肠畸形大鼠中支配直肠的骶副交感核的定量分析。

Quantitative analysis of sacral parasympathetic nucleus innervating the rectum in rats with anorectal malformation.

作者信息

Jia Huimin, Zhang Keren, Zhang Shucheng, Yuan Zhengwei, Bai Yuzuo, Wang Weilin

机构信息

Department of Paediatric Surgery, The 2nd Clinical College of China Medical University, Shenyang 110004, PR China.

出版信息

J Pediatr Surg. 2007 Sep;42(9):1544-8. doi: 10.1016/j.jpedsurg.2007.04.034.

Abstract

BACKGROUND/PURPOSE: The purpose of this experiment was to identify the neurons in the lumbosacral spinal cord involved in colon-rectal function and to compare normal and anorectal malformation of fetal rats.

METHODS

The authors quantified the sacral parasympathetic nucleus (SPN) innervation of the rectum by Fluorogold (FG) (Fluorochrome, Englewood, CO) retrograde tracing experiment in fetal rats with normal and anorectal malformation. Anorectal malformation was induced in rat fetuses by ethylenethiourea (ETU). The number of FG-labeled SPNs was scored and compared between male fetuses with or without malformation in the ETU-fed group and control groups.

RESULTS

The number of FG-labeled SPNs in the fetuses without a defect, with ETU injected but without any defects of the anorectum or neural tube, with low-type deformity, and with high-type deformity were (mean +/- SEM) 47.3 +/- 2.9, 45.6 +/- 3.2, 24.2 +/- 3.8, and 8.5 +/- 2.5, respectively. Fluorogold-labeled SPNs in the fetuses with high-type deformity were significantly fewer than those in fetuses without defects (P<.05) and in controls (P < .05).

CONCLUSIONS

These findings suggest that defective SPN innervation to the rectum is a primary anomaly that coexists with the alimentary tract anomaly in anorectal malformation during fetal development. The intrinsic neural deficiency is an important factor likely to contribute to poor postoperative anorectal function despite surgical correction of the malformation.

摘要

背景/目的:本实验旨在确定参与结肠直肠功能的腰骶脊髓中的神经元,并比较正常和肛门直肠畸形的胎鼠情况。

方法

作者通过荧光金(FG)(Fluorochrome公司,科罗拉多州恩格尔伍德)逆行追踪实验,对正常和肛门直肠畸形的胎鼠直肠的骶副交感核(SPN)神经支配进行量化。用乙硫脲(ETU)诱导大鼠胎儿出现肛门直肠畸形。对ETU喂养组和对照组中有或无畸形的雄性胎儿中FG标记的SPN数量进行评分和比较。

结果

无缺陷、注射ETU但无肛门直肠或神经管任何缺陷、低型畸形和高型畸形的胎儿中,FG标记的SPN数量(平均值±标准误)分别为47.3±2.9、45.6±3.2、24.2±3.8和8.5±2.5。高型畸形胎儿中荧光金标记的SPN明显少于无缺陷胎儿(P<0.05)和对照组(P<0.05)。

结论

这些发现表明,直肠的SPN神经支配缺陷是一种原发性异常,在胎儿发育过程中与肛门直肠畸形中的消化道异常并存。尽管对畸形进行了手术矫正,但内在神经缺陷是可能导致术后肛门直肠功能不良的一个重要因素。

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