Modelo de carcinogênese gástrica utilizando piloroplastia de Finney: estudo experimental em ratos

Abstract

-Background: The duodenogastric reflux has been implicated as a potential carcinogen for the stomach and esophagus and is one of the factors that may explain the development of gastric stump cancer. Experimental models of carcinogenesis in the stomach stump or in the duodenogastric anastomosis are well defined. Aim -To develop an experimental model of gastric carcinogenesis through the Finney pyloroplasty, evaluate the influence of ingestion of sodium nitrite in this model, analyze the concentrations of bile acids and the pH of the stomach. Methods -A hundred and ten Wistar rats were operated and divided into four groups: Group I (15 rats) underwent laparotomy (Sham group); Group II (15 rats) underwent laparotomy (Sham) and ingestion of sodium nitrite in drinking water; Group III (40 rats) submitted to the Finney pyloroplasty and Group IV (40 rats) submitted to the Finney pyloroplasty and ingestion of sodium nitrite in drinking water. After 50 weeks of surgery, the rats were sacrificed and samples collected for analysis of gastric pH, dosing of bile acids and histological analysis. Results -The immediate postoperative mortality was 9%, and during the experiment, 10 rats died. The control group (I) did not show gastric lesions; the control group with sodium nitrite (II) developed papillomas in the pre-stomach in 16.6%; the operated groups with pyloroplasty had adenomas in 10.3% in Group III and 14.2 % in Group IV, and adenocarcinoma in 55.1% in group III and 14.2% in Group IV. The implementation of glands into the submucosa and muscle in the area of anastomosis (mucosa deployment) was not sufficient criterion for deciding on the malignancy of the lesions, requiring the simultaneous presence of atypical cells. The concentration of bile acids in gastric juice was higher in Groups III and IV. The measurement of gastric pH was not different in both groups. Conclusion -1) The Finney pyloroplasty is suitable experimental model of gastric carcinogenesis; 2) it induced duodenogastric reflux; 3) the duodenogastric reflux served as a carcinogen for the stomach; 4) there was no relationship between pH and the development of gastric carcinoma; 5 ) sodium nitrite did not act as a carcinogen for the stomach of rats. ABCDDV/816RESUMO -Racional -O refluxo duodenogástrico tem sido implicado como potencial carcinógeno para o estômago e esôfago e é um dos fatores que podem explicar o desenvolvimento de câncer no coto gástrico. Modelos experimentais de carcinogênese no estômago ressecado ou nas gastrojejunoanastomoses estão bem definidos. Objetivos -Desenvolver um modelo experimental de carcinogênese gástrica através de piloroplastia à Finney, avaliar a influência da ingestão de nitrito de sódio nesse modelo, analisar as concentrações de ácidos biliares e o valor do pH gástrico. Métodos -Foram operados 110 ratos Wistar divididos em quatro grupos: Grupo I (15 ratos) submetidos à laparotomia (grupo Sham); Grupo II (15 ratos) submetidos à laparotomia (Sham) e à ingestão de nitrito de sódio na água de beber; Grupo III (40 ratos...

Influence of duodenogastric reflux in the gastric mucosa histological changes of rats infected with Helicobacter pylori

“…H. pylori infection in-duces chronic inflammation of the gastric mucosa, which leads to destruction of the protective barrier that coats the stomach mucosa, allowing the gastric acid to harm the mucosa, leading to the development of various types of neoplasms, though through unknown development mechanisms16 .In this study, there was predominance of benign proliferative lesions, with four malignant neoplasms located in the gastric antrum, at the pyloroplasty suture line. This location is the most common in experimental work that perform partial gastrectomy with Billroth II reconstruction or gastroenterostomy without gastric resection[17][18][19] .The sum of factors, such as the infectious process, inflammation and pyloroplasty, could provide a stimulus to cell proliferation. The increase in cell proliferation is one of the prerequisites for carcinogenesis.…”