Nitric oxide synthase distribution in the enteric nervous system of Hirschsprung's disease

Vanderwinden, Jean Marie; Laet, M H De; Schiffmann, Serge N.; Mailleux, Pierre; Lowenstein, Charles J.; Snyder, Solomon H.; Vanderhaeghen, J J

doi:10.1016/0016-5085(93)90938-9

Cited by 118 publications

(49 citation statements)

References 14 publications

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“…2 Esophageal webs could also be considered as a variety of CES, as described by Vergos et al 9 Motility abnormality was associated with CES in two adult cases, 10 where the abnormality was due to nitrinergic denervation with the lack of nitric acid inhibitory effect. Similar explanation has been given in other disorders, such as achalasia of cardia, 11,12 Hirschsprungs' disease, 13,14 and hypertrophic pyloric stenosis. What all these have in common is a failure of relaxation of the affected segment.…”

Section: Discussionsupporting

confidence: 68%

Isolated Congenital Esophageal Stenosis: A Case Report and Review of the Literature

Al-Malki

Ibrahim

2000

Ann Saudi Med

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Section: Discussionsupporting

confidence: 68%

Isolated Congenital Esophageal Stenosis: A Case Report and Review of the Literature

Al-Malki

Ibrahim

2000

Ann Saudi Med

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“…11 This view is supported by the fact that pyloric tissue samples from patients with hypertrophic pyloric stenosis show deficiency of nitrergic innervation. 26 However, it is unknown if nNOS −/− mice fully support phenotype of hypertrophic pyloric stenosis. The gastric phenotype in nNOS −/− mice has also been proposed to resemble diabetic gastroparesis 6,7 and deficiency of nitrergic neurotransmission has been reported in experimental diabetic gastroparesis.…”

Section: Discussionmentioning

confidence: 99%

Pyloric Sphincter Dysfunction in nNOS−/− and W/Wv Mutant Mice: Animal Models of Gastroparesis and Duodenogastric Reflux

2008

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“…Progressive maturation of ENS was further evidenced using antibody recognizing an epitope common to the three subnunits of the cytoskeletal neuronal protein NF and nNOS, a nonadrenergic noncholinergic mediator of the nervous system produced by enteric neurons with inhibitory functions (14,15). The latter protein plays a key role in the regulation of intestinal motility (16,17). Both markers had a similar pattern of expression during development, being first detected at the beginning of the second trimester.…”

Section: Discussionmentioning

confidence: 99%

Fetal Intestinal Obstruction Induces Alteration of Enteric Nervous System Development in Human Intestinal Atresia

et al. 2004

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Intestinal motility disorders are a major cause of morbidity after surgical repair of intestinal atresia of unknown mechanism. We hypothesized that interruption of antenatal peristalsis may disturb the normal development of the enteric nervous system. Using a series of neuronal (synaptophysin, neuronal nitric oxide synthase, neurofilaments) and nonneuronal markers (glial acidic fibrillary protein and c-Kit) and immunohistochemistry, we have defined developmental steps of the enteric nervous system in normal intestine (12 fetuses, 15 children, and 4 adults) and their alterations above and below the obstacle in 22 human intestinal atresia compared with age-matched controls. Antisynaptophysin antibody revealed the progressive conversion of the myenteric plexus from a continuous belt into regularly spaced ganglions during normal fetal gut development and, by contrast, the significantly delayed appearance of individual neuronal ganglions in the distal segments of atresia (p Ͻ 0.05). Staging using three other markers for neuronal (neurofilaments and neuronal nitric oxide synthase) and nonneuronal cells (glial acidic fibrillary protein) confirmed that maturation of the myenteric plexus was significantly delayed below atresia (p Ͻ 0.01). These results indicate that intestinal atresia impairs the development of the enteric nervous system and provide an anatomical substrate for the motility disorders observed after surgical repair. They point to the role of peristalsis in normal gut development and suggest that stimulation of peristalsis might be used to accelerate recovery. Intestinal atresia is a common gut congenital disease with a prevalence of 2.8 for 10,000 births (1), detected by prenatal ultrasonography in the second or third trimester and confirmed at birth by intestinal obstruction. Treatment must be performed just after birth and consists of surgical resection of the atretic segment followed by primary anastomosis. Operative techniques and postoperative parenteral nutrition have improved the outcome, but prolonged intestinal motility disorders remain common in the postoperative period, even in the absence of any mechanical lesions (2). Although a dysfunction of the ENS has been suggested, the physiopathology of the motility disorders remains unknown (3,4).ENS comprises two main plexuses and schematically it can be assumed that the myenteric or Auerbach's plexus plays a major role in the regulation of motility and that the submucous or Meissner's plexus ensures regulation of intestinal secretion/ absorption (5,6). Intestinal motility appears early at 16 wk gestation (7) in fetal life and likely supports the nutritional function of the gut before birth (8,9). Intestinal atresia, by 0031-3998/04/5606-0975 PEDIATRIC RESEARCH Vol. 56, No. 6, 2004 Copyright © 2004 Printed in U.S.A. ABSTRACT975

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Nitric oxide synthase distribution in the enteric nervous system of Hirschsprung's disease

Cited by 118 publications

References 14 publications

Isolated Congenital Esophageal Stenosis: A Case Report and Review of the Literature

Isolated Congenital Esophageal Stenosis: A Case Report and Review of the Literature

Pyloric Sphincter Dysfunction in nNOS−/− and W/Wv Mutant Mice: Animal Models of Gastroparesis and Duodenogastric Reflux

Fetal Intestinal Obstruction Induces Alteration of Enteric Nervous System Development in Human Intestinal Atresia

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