Morphology and mucosal biochemistry of gastroschisis intestine in urine-free amniotic fluid

Albert, A; Margarit, J; Victoria, Julia; Sancho, M. A.; Galan, Xavier; López, Dolores; Morales, Leonardo Fabio

doi:10.1016/s0022-3468(03)00271-9

Cited by 17 publications

(17 citation statements)

References 13 publications

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“…0.001 and p = 0.015, respectively) in both groups, results that were comparable to those of Albert et al [26] . With a similar behavior to IL, D-II also presented significant differences when compared to measures of both groups, that is D-II in gastroschisis fetuses of E18.5 was smaller than in gastroschisis fetuses of E19.5 (p !…”

Section: Discussionsupporting

confidence: 91%

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Maturity of the Myenteric Plexus Is Decreased in the Gastroschisis Rat Model

França¹,

Langone²,

Hoz³

et al. 2007

Fetal Diagn Ther

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Background: Amniotic fluid (AF) and its components, such as fetal urine and meconium, may lead to intestinal alterations in gastroschisis, which cause immaturity of the myenteric plexus and consequent intestinal hypomotility and malabsorption. In this study we identified morphological and histological alterations of the intestine and the myenteric plexus with two different times of exposure to AF. Methods: The experimental gastroschisis was achieved at two different gestational ages, on day 18.5 (E18.5) and day 19.5 (E19.5) of gestation, in fetal rats which were divided into 3 subgroups: control, sham and gastroschisis. We measured fetal body weight (BW), intestinal weight (IW) and intestinal length (IL). The layers of intestinal wall and myenteric plexus were evaluated by hematoxylin and eosin staining (HE staining) and immunofluorescence (α-internexin), respectively. Results: BW was not significantly different among the control, sham and gastroschisis groups at both ages. IW and IL were larger and shorter, respectively, in the gastroschisis fetuses (p < 0.001) at both ages. Intestinal diameters and wall layers presented significant differences among control, sham and gastroschisis fetuses at both ages (p < 0.001), but the time of exposure to AF compromised the serous membrane, D-II (diameter II, p < 0.001) and IL (p = 0.001). α-Internexin presented more intensive immunoreactivity in gastroschisis fetuses at E18.5. Conclusions: In gastroschisis, the longer the time of exposure to AF, the more severe bowel impairment will be, especially with regard to IL and the serous layer, and the more immature the myenteric plexus will be.

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Section: Discussionsupporting

confidence: 91%

“…0.001), in both the E18.5 and E19.5 groups (p = 0.035), as was also found in the rabbit [26] and chicken [28] models. Once again, these results show the deleterious effects in the course of gestation on bowel loops, mainly in the serous layer.…”

Section: Discussionsupporting

confidence: 77%

Maturity of the Myenteric Plexus Is Decreased in the Gastroschisis Rat Model

França¹,

Langone²,

Hoz³

et al. 2007

Fetal Diagn Ther

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show abstract

“…The duration and severity of neonatal gut dysfunction in infants with gastroschisis have been linked to the degree of intestinal damage sustained in utero. From both experimental animal models and observations in affected infants, intestinal injury, and particularly peel formation, in gastroschisis has been attributed to either meconium [9,10] or urine [11] in amniotic fluid. A few authors have rejected the concept that amniotic fluid is involved in the pathogenesis of gut damage in gastroschisis [12], and others have been so convinced by the experimental data that they have proposed amniotic fluid infusion or exchange as a beneficial intervention [12,14].…”

Section: Discussionmentioning

confidence: 99%

A randomized controlled trial of elective preterm delivery of fetuses with gastroschisis

Logghe

Mason

Thornton

et al. 2005

Journal of Pediatric Surgery

131

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“…The intestinal dysfunction in Gx is believed to result from both loss of contractility and poor absorptive capacity because of mucosal villous atrophy and immaturity of the mucosal enzymatic systems [22]. The etiology of these changes in Gx has been attributed to a variety of causes, including both amniotic fluid exposure and intrauterine ischemia caused by gradual constriction of the bowel at the abdominal wall defect [23].…”

Section: Discussionmentioning

confidence: 99%