O refluxo duodeno-gástrico (RDG), através do piloro, induz lesões proliferativas gástricas em ratos?

Abstract

Objetivo: Estudar o desenvolvimento de lesões proliferativas na mucosa gástrica de ratos Wistar submetidos ao refluxo duodeno-gástrico (RDG) através do piloro e, também, avaliar os efeitos da interrupção do RDG sobre o desenvolvimento das mesmas. Métodos: Constituíram-se três grupos experimentais: No CT (n = 20) os ratos foram submetidos a uma gastrotomia; nos grupos RDG54 (n = 16) e RDG36 (n = 14) realizou-se a indução do RDG e, somente no último, interrompeu-se o RDG após 36 semanas. O RDG foi obtido através da realização de anastomose entre o jejuno proximal e a parede gástrica anterior, seguido por secção completa e fechamento das bocas distal e proximal do jejuno a cerca de 1cm antes do início da gastroenteroanastomose. Na 54ª semana do seguimento, todos os ratos foram submetidos à eutanásia. Resultados: Diagnosticaram-se três tipos de lesões proliferativas: na mucosa glandular, a hiperplasia adenomatosa e o adenocarcinoma e, no epitélio escamoso, a hiperplasia escamosa. No grupo CT, não se diagnosticaram lesões proliferativas. Na região da mucosa pilórica dos grupos RDG54 e RDG36, a incidência da hiperplasia adenomatosa foi, respectivamente, de 68,75% e 50% (p > 0,30), enquanto na região da gastroenteroanastomose, de 43,75% no RDG54 e 85,71% no RDG36 (p < 0,05). No epitélio escamoso, a incidência da hiperplasia escamosa no RDG54 e RDG36 foi, respectivamente, de 62,5% e 14,2% (p < 0,001). O adenocarcinoma foi diagnosticado na região da anastomose de uma única peça histológica do RDG54. Através de um sistema de análise digital, determinaram-se as áreas da hiperplasia adenomatosa. Na região da mucosa pilórica, obteve-se mediana de 8,583mm² no RDG54 e de 0,2690mm² no RDG36 (p < 0,001). Na gastroenteroanastomose, obteve-se zero no RDG54 e 0,5295mm² no RDG36 (p > 0,50). Conclusões: O RDG propiciou o desenvolvimento de lesões proliferativas, predominantemente benignas. A interrupção do RDG refreou o crescimento da área da hiperplasia adenomatosa na mucosa pilórica e diminuiu a incidência da hiperplasia escamosa. Na região da gastroenteroanastomose, o procedimento cirúrgico favoreceu a manutenção do processo prolifera tivo, mesmo após a interrupção do RDG através do piloro.<br>Objective: The aims of this study were to investigate the development of proliferating lesions in the gastric mucosa of male Wistar rats induced by duodenogastric reflux (DGR) through the pylorus, and also to study the effects of DGR interruption on the development of proliferating lesions. Methods: Three groups were randomly established: Sham <FONT FACE=Symbol>-</FONT> 20 rats were submitted to a gastrotomy at the anterior gastric wall; DGR54 <FONT FACE=Symbol>-</FONT> 16 rats were operated to create the DGR through the pylorus; DGR36 <FONT FACE=Symbol>-</FONT> 14 rats were submitted to the same surgical procedure to create DGR through the pylorus, but, in the 36th week the DGR was interrupted. For the achievement of the DGR, an anastomosis was made between the proximal jejunum and the anterior gastric wall, then the jejunum was divided 1cm ...

Gastric proliferative lesions induced by duodenogastric reflux in rats

“…It was much more frequent in group III, in which the animals had the duodenum closed, so that the duodenal content had to pass through the stomach. Its benign characteristics suggest that if the animal were operated again AH might regress, as previously demonstrated by other authors 19,20 . In the squamous epithelium that lines the proximal third of the stomach the presence of squamous hyperplasia was found, with a frequency that did not significantly differ between the animals in groups II and III.…”

“…In 2002, Rodrigues et al 20 investigated the effect of duodenal secretion reflux in groups of Wistar rats, with 3 experimental groups: G1 (control), G2 (submitted to gastrojejunal anastomosis and 2 weeks later to ligature of the afferent loop, deviating secretions through the pylorus) and G3 (gastrojejunal anastomosis; after the 36 th week, alimentary transit was reestablished by latero-lateral anastomosis between the afferent and efferent loops. After a period of 54 weeks, the author concluded that the reflux through the pylorus favored the development of predominantly benign proliferative lesions in the gastric mucosa.…”

Does troncular vagotomy modify the proliferative gastric lesions induced in rats by duodenogastric reflux<A HREF="#back2"></A>?<A HREF="#back2"></A>

“…The glandular hyperplasia would increase mucus production in order to adapt the mucosa to the deleterious environment of reflux. In a previous study 9 , we have demonstrated direct correlation between the glandular hyperplasia and duodenogastric reflux, since the proliferative lesions were reversible with interruption of reflux. In the present study troncular vagotomy (TV), alone, did not induce any lesions in the gastric mucosa and it did not modify the morphologic picture of the proliferative lesions induced by DGR through the pylorus.…”

“…The deleterious effects of biliopancreatic secretions on the gastric mucosa have been investigated by several authors 6,7,8 . In a previous study 9 , we have observed direct correlation between duodenogastric reflux and the development of epithelial proliferative lesions in the pyloric mucosa. However, the lesions induced by the duodenogastric reflux were a benign condition, since they did not present cellular atypia or mural invasion and were reversible with interruption of duodenogastric reflux.…”

“…These lesions could be related to the prolonged contact of the gastric mucosa with the components of bile and pancreatic secretion. They probably result from the deleterious action of the DGR components on the mucus layer of the gastric epithelium 6,8,9,10 . The detergent action of the components of bile can modify the permeability of the mucosa enhancing back-diffusion of chemical substances into the mucosa.…”