RESUMO
To date, intrinsic obstructions of the duodenum have been explained by the "solid core" theory, described by Tandler in 1902 (Morphol Jahrb 29:187-216, 1902). This study aimed to evaluate the epithelial occlusion of rat duodenum during embryonic development, through optical microscopy and computerized three-dimensional reconstruction. The Wistar rat embryos used in this study had 13, 14, 15, and 16 days of gestation. This corresponds to human embryos with 33, 40, 44, and 52 days of development, which is between the fifth and eighth week. The study included 12 embryos studied by optical microscopy, and four by three-dimensional reconstruction (those with 13, 14, 15, and 16 days). Through optical microscopy, an intense epithelial proliferation was observed in the gestation embryo of 13 days, with no occlusion of the opening of the duodenum. In the embryos with 14, 15, and 16 days of gestation, an increase in diameter of the duodenum was observed along with intestinal development. Through three-dimensional reconstruction, it was observed that the opening of the digestive tube of rat embryos with 13-16 days of gestation is never obstructed by epithelial proliferation, although it may follow a sinuous path. This study concludes that the "solid core" phase described by Tandler does not occur in the embryonic development of rat duodenum.
Assuntos
Duodeno/embriologia , Imageamento Tridimensional/métodos , Animais , Modelos Animais de Doenças , Duodeno/citologia , Feminino , Seguimentos , Masculino , Gravidez , Ratos , Ratos WistarRESUMO
Etiopathogenesis of biliary atresia remains unknown. Among several theories, one proposes that the disorder may be caused by the toxic effect of monohydroxy bile acids on fetal and neonatal hepatobiliary system. In this paper we evaluated toxic effects produced by ingestion of cholic acid, a trihydroxy bile acid, and lithocholic acid, a monohydroxy bile acid in the hepatobiliary system of a hamster during gestational and perinatal periods. A diet composed by 0.5% cholic acid and 0.25% lithocholic acid was administrated to pregnant hamsters. Liver and bile ducts of the adult and newborn animals were analyzed to point out the changes induced by these acids after birth. Because hamsters and humans have a similar bile metabolism, these animals were eligible for the study. The ingestion of 0.5% lithocholic acid, during hamster's gestation, caused maternal intense ductal/ductular proliferation, inflammatory signs, hepatic cells degeneration and regeneration, hyperplasia of extra hepatic ducts epithelium, and abortion. Both 0.5% cholic acid and 0.25% lithocholic acid ingested by pregnant hamsters, caused ductal/ductular proliferation and hepatobiliary inflammatory damage in a different degree of intensity in adult animals and mild intensity in the young; and also the number of the young was reduced in the litter. We found that the ingestion of these bile acids by hamsters, during gestational period caused different degrees of toxicity on maternal and neonatal hepatobiliary systems. The histopathologic findings observed in biliary atresia patients could not be found in newborn hamsters. New experimental models are needed in the attempt to establish a correlation of these acids with neonatal cholestatic diseases.
Assuntos
Sistema Biliar/efeitos dos fármacos , Ácido Cólico/toxicidade , Ácido Litocólico/toxicidade , Fígado/efeitos dos fármacos , Administração Oral , Animais , Animais Recém-Nascidos , Atresia Biliar/etiologia , Ácido Cólico/administração & dosagem , Cricetinae , Feminino , Ácido Litocólico/administração & dosagem , Masculino , Troca Materno-Fetal , GravidezRESUMO
Objetivo: reproduzir, experimentalmente, em ratos por meio do inibidor da enzima óxido nítrico sintase (ONS - L-NAME), os achados histopatológicos correspondentes a estenose hipertrófica do piloro da infância (EHPI). Métodos: para reproduzir o modelo de inibição de ONS na produção de EHPI, administrou-se L-NAME em ratas grávidas, a partir do 14§ dia gestacional (grupo L-NAME), comparando-se com uma gestação de controle. Após o nascimento, todos os ratos do grupo L-NAME foram mantidos sob inibição da ONS até o 42§ de vida, quando foram sacrificados. Os filhotes da gestação de controle, em que nenhuma droga foi administrada, foram também sacrificados com 42 dias de vida. Os animais e as visceras foram analisados e pesados. A região foi preparada tecnicamente e observada em microscopia de luz. Resultados: em comparação com os animais de controle, os L-NAME tiveram peso corporal e instestinal menor e peso gástrico maior. Nos animais L-NAME a microscopia de luz evidênciou hipertrofia da camada circular do músculo liso do piloro. Conclusão: este trabalho reproduziu um modelo experimental de estudo da estenose hipertrófica do piloro e comprovou, neste modelo a associação da ausência da ON sintase na musculatura do piloro