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Article: Deficient motor innervation of the sphincter mechanism in fetal rats with anorectal malformation: A quantitative study by fluorogold retrograde tracing

TitleDeficient motor innervation of the sphincter mechanism in fetal rats with anorectal malformation: A quantitative study by fluorogold retrograde tracing
Authors
KeywordsAnal sphincter mechanism
Anorectal malformation
Motor neuron innervation
Issue Date2003
PublisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/jpedsurg
Citation
Journal Of Pediatric Surgery, 2003, v. 38 n. 9, p. 1383-1388 How to Cite?
AbstractBackground/Purpose: Deficiency of motoneuron innervation to the sphincter mechanism has been described in patients with anorectal malformation. Whether this event is primary or secondary remains unclear. Methods: The authors quantified the motoneuron innervation of the sphincter mechanism by Fluorogold (FG) retrograde tracing experiment in fetal rats with anorectal malformation. Anorectal malformation was induced in rat fetuses by ethylenethiourea (ETU). Serial longitudinal sections encompassing the whole width of lumbosacral spinal cord were examined. The number of FG-labelled motoneurons were scored and compared between male fetuses with or without malformation in the ETU-fed group and normal controls. Results: The number of FG-labelled motoneurons in the fetuses without defect, with imperforate anus (IA), with neural tube anomalies (NTA), with combined IA and NTA, and normal controls were determined to be (mean ± SEM) 109.13 ± 37.88, 55.05 ± 25.85, 48.20 ± 30.34, 54.43 ± 28.55, and 135.22 ± 28.78, respectively. FG-labelled motoneurons in the fetuses with IA, NTA, and combined IA and NTA are significantly fewer than that in fetuses without defects (P < .05) and in normal controls (P < .005). Conclusions: These findings suggest that defective motoneuron innervation to the sphincter mechanism 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 anorectal malformation. © 2003 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/83556
ISSN
2015 Impact Factor: 1.733
2015 SCImago Journal Rankings: 0.802
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYuan, ZWen_HK
dc.contributor.authorLui, VCHen_HK
dc.contributor.authorTam, PKHen_HK
dc.date.accessioned2010-09-06T08:42:26Z-
dc.date.available2010-09-06T08:42:26Z-
dc.date.issued2003en_HK
dc.identifier.citationJournal Of Pediatric Surgery, 2003, v. 38 n. 9, p. 1383-1388en_HK
dc.identifier.issn0022-3468en_HK
dc.identifier.urihttp://hdl.handle.net/10722/83556-
dc.description.abstractBackground/Purpose: Deficiency of motoneuron innervation to the sphincter mechanism has been described in patients with anorectal malformation. Whether this event is primary or secondary remains unclear. Methods: The authors quantified the motoneuron innervation of the sphincter mechanism by Fluorogold (FG) retrograde tracing experiment in fetal rats with anorectal malformation. Anorectal malformation was induced in rat fetuses by ethylenethiourea (ETU). Serial longitudinal sections encompassing the whole width of lumbosacral spinal cord were examined. The number of FG-labelled motoneurons were scored and compared between male fetuses with or without malformation in the ETU-fed group and normal controls. Results: The number of FG-labelled motoneurons in the fetuses without defect, with imperforate anus (IA), with neural tube anomalies (NTA), with combined IA and NTA, and normal controls were determined to be (mean ± SEM) 109.13 ± 37.88, 55.05 ± 25.85, 48.20 ± 30.34, 54.43 ± 28.55, and 135.22 ± 28.78, respectively. FG-labelled motoneurons in the fetuses with IA, NTA, and combined IA and NTA are significantly fewer than that in fetuses without defects (P < .05) and in normal controls (P < .005). Conclusions: These findings suggest that defective motoneuron innervation to the sphincter mechanism 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 anorectal malformation. © 2003 Elsevier Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/jpedsurgen_HK
dc.relation.ispartofJournal of Pediatric Surgeryen_HK
dc.subjectAnal sphincter mechanismen_HK
dc.subjectAnorectal malformationen_HK
dc.subjectMotor neuron innervationen_HK
dc.titleDeficient motor innervation of the sphincter mechanism in fetal rats with anorectal malformation: A quantitative study by fluorogold retrograde tracingen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-3468&volume=38&issue=9&spage=1383&epage=1388&date=2003&atitle=Deficient+motor+innervation+of+the+sphincter+mechanism+in+fetal+rats+with+anorectal+malformation:+a+quantitative+study+by+fluorogold+retrograde+tracingen_HK
dc.identifier.emailLui, VCH: vchlui@hkucc.hku.hken_HK
dc.identifier.emailTam, PKH: paultam@hkucc.hku.hken_HK
dc.identifier.authorityLui, VCH=rp00363en_HK
dc.identifier.authorityTam, PKH=rp00060en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/S0022-3468(03)00401-9en_HK
dc.identifier.pmid14523825-
dc.identifier.scopuseid_2-s2.0-0141454028en_HK
dc.identifier.hkuros80956en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0141454028&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume38en_HK
dc.identifier.issue9en_HK
dc.identifier.spage1383en_HK
dc.identifier.epage1388en_HK
dc.identifier.isiWOS:000185741600021-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridYuan, ZW=8672008500en_HK
dc.identifier.scopusauthoridLui, VCH=7004231344en_HK
dc.identifier.scopusauthoridTam, PKH=7202539421en_HK

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