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.
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.
Authors: Tao Zhang; Hai Lan Zhang; Da Jia Wang; Xiao Bing Tang; Hui Min Jia; Yu Zuo Bai; Zheng Wei Yuan; Wei Lin Wang Journal: Int J Colorectal Dis Date: 2010-08-05 Impact factor: 2.571