| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 4159660 | Journal of Pediatric Surgery | 2007 | 5 Pages |
Background/PurposeThe 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 fetalrats.MethodsThe 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.ResultsThe 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 inthe fetuses with high-type deformity were significantly fewer than those in fetuses without defects (P<.05) and in controls (P < .05).ConclusionsThese 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.
