A new rodent experimental model of esophageal atresia and tracheoesophageal fistula: Preliminary report

Díez-Pardo, Juan A.; B, Qi; Navarro, Carmen; Tovar, Juan A.

doi:10.1016/s0022-3468(96)90482-0

Cited by 128 publications

(71 citation statements)

References 12 publications

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“…These results were in line with previous rat studies in which malformation of the foregut and caudal eminence derived organs, including esophageal and intestinal atresia, tracheoesophageal fistula, renal and anorectal anomalies, were induced by embryonic exposure to adriamycin (16,26,27). This study not only replicated embryonic toxicity of adriamycin in a species other than rodents, but also strengthened conclusion of previous studies in three aspects.…”

Section: Discussionsupporting

confidence: 92%

Caudal Regression and Tracheoesophageal Malformation Induced by Adriamycin: A Novel Chick Model of VATER Association

et al. 2009

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VATER association represents a cluster of Vertebral, Anal, Tracheo-Esophageal, Radial and Renal malformations, and caudal regression syndrome is an entity consisting of a spectrum of congenital anomalies of lower spine and hips associated with genitourinary and lower limb defects. The concurrence of various malformations may be explained by a common defect in blastogenesis, but direct evidence is yet to be accumulated. Here, by the use of autofluorescence and the teratogenic effect of adriamycin, we demonstrated that adriamycin administered to eggs of White Leghorns distributes to the caudal portion of the embryo and foregut epithelium and induces caudal regression and tracheal and pulmonary agenesis. The induction of caudal regression syndrome-like anomaly was developmental stage and dose dependent. Embryos with caudal regression demonstrated tracheoesophageal anomalies, one of the defects included in VATER association. The stages at which anomalies were produced corresponded to that of human embryos between days 22 and 26 (Carnegie stages 10 -11). In view of the antitumor activity of adriamycin by intercalating to double-stranded DNA of undifferentiated cells undergoing rapid cell division, it is possible that adriamycin had preferentially attacked cells in the caudal end where pronounced proliferation takes place during this narrow period of greatest susceptibility. (Pediatr Res 65: 607-612, 2009)

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Section: Discussionsupporting

confidence: 92%

Caudal Regression and Tracheoesophageal Malformation Induced by Adriamycin: A Novel Chick Model of VATER Association

et al. 2009

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“…In our study, histological assessments of the EA and TEF and control specimens essentially confirmed previously reported observations in an adriamycin rat model [2,3,15]. In addition, Cheng et al [14] found neuropeptide abnormality in the lower esophagus morphological abnormality of the distal esophagus.…”

Section: Discussionsupporting

confidence: 91%

“…The adriamycin rat model produces EA and TEF similar to the most common human anatomic variant allows better understanding pathophysiology of EA and associated anomalies [1,2,15]. In this experimental study we have found several histological and morphological changes in distal esophagus, tracheobronchial tree, and lung parenchyma.…”

Section: Discussionmentioning

confidence: 62%

Esophageal, Tracheal and Pulmonary Parenchymal Alterations in Experimental Esophageal Atresia and Tracheoesophageal Fistula

Otcu

Kaya²,

Öztürk³

et al. 2002

Eur Surg Res

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Pulmonary complications are among the most important causes of morbidity and mortality in neonates with esophageal atresia and tracheofistula. We aimed to investigate the possible causes of respiratory complications encountered in esophageal atresia (EA) and tracheoesophageal fistula (TEF) in an experimental model. Sprague-Dawley fetal rats treated with adriamycin were used for the experiment. Time mated pregnant rats were given 1.75 mg/kg of adriamicyn intraperitoneally on days 6–9 of gestation. The fetuses were sacrified on day 21, weighed, and dissected under the surgical microscope. The animals were divided into four groups: (1) control group; (2) saline-injected group; (3) adriamycin-induced EA group, and (4) adriamycin administered but without development of EA. The lungs, esophagus, and trachea were excised and underwent histological examination. The mucosa of distal esophagus was thickened (p < 0.05); the submucosa was thinner (p < 0.05); and the muscular layer was thickened (p < 0.05) in fetuses with EA and TEF. In adriamycin-treated rats, in which EA and TEF developed, tracheal cartilage was loosened and formed into a D or C shape. The cartilage was fragmented into several segments on transverse sections in most fetuses. Alveolar septa were thin in lungs of fetus with EA and TEF (p < 0.05), without any fibrosis or evidence of parenchymal abnormality microscopically. Our findings suggest that respiratory complications may contribute to structural lesions in the trachea and particularly in the distal esophagus but not in the pulmonary parenchyma itself.

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“…Most hy-potheses of the pathogenesis of ATDs (Bremer, 1952;McLetchie et al, 1954;Nathan, 1959;Nobuhara et al, 1997) do not account for the range and variety of ATDs seen in the gastrointestinal tract and none explain the coexistence of EA-TEF and FgD. The observation of esophageal duplication cysts in rat fetuses with EA-TEF induced by intraperitoneal injection of Adriamycin into timed-pregnant rats (Diez-Pardo et al, 1996) prompted us to investigate whether there is any demonstrable relationship between EA-TEF and FgD, and to study the embryogenesis of FgD.…”

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confidence: 99%

Evidence of a common pathogenesis for foregut duplications and esophageal atresia with tracheo‐esophageal fistula

Beasley

Williams

2001

Anat. Rec.

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The pathogenesis of the alimentary tract duplications, including foregut duplications (FgD) remains speculative. The accidental finding of FgD in fetal rats with esophageal atresia and tracheoesophageal fistula (EA-TEF) induced by Adriamycin provided an animal model to investigate a possible relationship between these two entities. Timed-pregnant rats were intraperitoneally injected with Adriamycin (1.75 mg/kg) on gestational Days 6 to 9. Their embryos were harvested by Caesarean section from gestational Days 14 to 21. Forty-six of embryos were processed and serially sectioned in the transverse or sagittal planes. EA-TEF occurred in 43/46 (93%) embryos of which 11 (24%) were found to have an associated FgD located at the level where the esophagus was absent. Six FgDs communicated with the foregut or the trachea. Five noncommunicating FgDs were located between the foregut and the vertebral column. In the control embryo, the notochord was located in the centre of the vertebral column from Day 11 of the gestation. In Day 14, 15 and 16, however, embryos exposed to Adriamycin, an abnormal notochord or branch frequently was located within the mesenchyme of the maldeveloped foregut or attached to the duplication cyst. In some, it appeared that the notochord was drawing the cyst-like structure away from the foregut. The present study confirms that duplications adjacent to the esophagus arise from the foregut and that failure of the foregut to detach from the notochord at the normal time may contribute to the development of foregut duplications. Anat Rec 264: [93][94][95][96][97][98][99][100] 2001.

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A new rodent experimental model of esophageal atresia and tracheoesophageal fistula: Preliminary report

Cited by 128 publications

References 12 publications

Caudal Regression and Tracheoesophageal Malformation Induced by Adriamycin: A Novel Chick Model of VATER Association

Caudal Regression and Tracheoesophageal Malformation Induced by Adriamycin: A Novel Chick Model of VATER Association

Esophageal, Tracheal and Pulmonary Parenchymal Alterations in Experimental Esophageal Atresia and Tracheoesophageal Fistula

Evidence of a common pathogenesis for foregut duplications and esophageal atresia with tracheo‐esophageal fistula

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