Kaoping Guan1, Hui Li, Yang Fan, Weilin Wang, Zhengwei Yuan. 1. Department of Pediatric Surgery, Key Laboratory of Health Ministry for Congenital Malformation, Shengjing Hospital, China Medical University, Shenyang 110004, China.
Abstract
BACKGROUND: Defects of the pelvic nerve innervation of levator ani muscle are associated with poor postoperative anorectal function in patients with anorectal malformation (ARM). We have previously shown deficient development of motoneurons innervating the levator ani muscle in rats with ARM. In this study we investigate whether there is a deficiency in the development of sensory neurons that innervate the levator ani muscle in rats with ARM. METHODS: ARM was induced by ethylenethiourea (ETU) in fetal rats. Retrograde tracer fluorogold (FG) was injected into the levator ani muscle. Serial transverse sections encompassing the entire length of the lumbosacral spinal cord were examined. The number of FG-labeled sensory neurons was scored and compared between fetuses with ARM and normal fetuses. RESULTS: The number of FG-labeled sensory neurons innervating the levator ani muscle in normal control fetuses, ETU-fed fetuses with no malformation, low type of imperforate anus, high type of imperforate anus, and high type of imperforate anus combined with neural tube defects were determined to be (mean +/- SEM) 11,804 +/- 2362, 10,429 +/- 1708, 2886 +/- 705, 1026 +/- 425, and 964 +/- 445, respectively. FG-labeled sensory neurons in fetuses with imperforate anus with or without neural tube defects were significantly fewer than in control and ETU-fed fetuses without malformation (p < 0.05). CONCLUSIONS: Defective sensory neurons innervating the levator ani muscle is a primary anomaly that coexists with the alimentary tract anomaly in ARM during fetal development. Nerve innervation deficiency of the pelvic muscles contributes to the poor postoperative anorectal functions in ARM patients.
BACKGROUND: Defects of the pelvic nerve innervation of levator ani muscle are associated with poor postoperative anorectal function in patients with anorectal malformation (ARM). We have previously shown deficient development of motoneurons innervating the levator ani muscle in rats with ARM. In this study we investigate whether there is a deficiency in the development of sensory neurons that innervate the levator ani muscle in rats with ARM. METHODS: ARM was induced by ethylenethiourea (ETU) in fetal rats. Retrograde tracer fluorogold (FG) was injected into the levator ani muscle. Serial transverse sections encompassing the entire length of the lumbosacral spinal cord were examined. The number of FG-labeled sensory neurons was scored and compared between fetuses with ARM and normal fetuses. RESULTS: The number of FG-labeled sensory neurons innervating the levator ani muscle in normal control fetuses, ETU-fed fetuses with no malformation, low type of imperforate anus, high type of imperforate anus, and high type of imperforate anus combined with neural tube defects were determined to be (mean +/- SEM) 11,804 +/- 2362, 10,429 +/- 1708, 2886 +/- 705, 1026 +/- 425, and 964 +/- 445, respectively. FG-labeled sensory neurons in fetuses with imperforate anus with or without neural tube defects were significantly fewer than in control and ETU-fed fetuses without malformation (p < 0.05). CONCLUSIONS: Defective sensory neurons innervating the levator ani muscle is a primary anomaly that coexists with the alimentary tract anomaly in ARM during fetal development. Nerve innervation deficiency of the pelvic muscles contributes to the poor postoperative anorectal functions in ARM patients.