Jan 2021
Vladimir Leonidovich MartynovCorresponding author
Doctor of Medical Sciences, Associate Professor, National Research Nizhny Novgorod State University named after N.I. Lobachevsky (UNN), Russia
The presence of numerous complaints of a gastroenterocolitic nature in patients with proven NBZ and CNDP and a sharp regression of these complaints after surgical correction of NBZ and CNDP allows us to conclude that the causes of these pathological manifestations are the failure of the Bauhinia valve and chronic violation of the duodenal patency, and the most adequate surgical aid for elimination of clinical manifestations of reflux disease is bauginoplasty with simultaneous duodenojejunostomy.
Jun 2016 DOI 10.14302/issn.2574-4526.jddd-16-1101
A. M. Herbella FernandoCorresponding author
Department of Surgery, Escola Paulista de Medicina, Federal University of Sao Paulo, São Paulo, Brazil
Background/Aims: Esophageal motor abnormalities are frequently found in patients with gastroesophageal reflux disease. The effect of bile in esophageal dysmotility is probably secondary to mucosal signaling to the muscular layer and not a transmural process. This study aims to identify the mucosa-muscular signaling path by receptors blockage in an experimental study. Methods: Fifteenguinea pig esophagi were isolated and ex-vivo esophageal contractility was assessed with force transducers. The esophagi were incubated in 100 µM ursodeoxycholic acid for 1 hour and 5 sequential contractions induced by 40 mM KCl spaced by 5 minutes were measured. After 30 minutes, esophagi specimens were incubated in 3 different smooth-muscle contraction antagonists: atropine (1µM) in 5, suramin (1µM) in 5 and genistein (1µM) in 5. The same protocol for contractions was repeated. Values are expressed as mean ± standard deviation and encompass the mean of five stimuli. Experimental procedures were approved by the University Institutional Review Board. Results: Contraction amplitudes after bile incubation but before antagonist incubation were 1.6±0.6 g, 1.2±0.8 g, and 1.2±0.4 g for atropine, suramin and genistein, respectively. Mean contraction amplitudes after antagonists instillation were 1.2±0.6 g, 1.4±0.5 g, 0.9±0.2 g, respectively. There was no different in contraction amplitude before and after instillation of atropine (p=0.188), suramin (p=0.488) or genistein (p=0.079). Conclusion: Our results show that blockage of cholinergic (atropine), purinergic (suramin) or tyrosine kinase (genistein) paths do not change esophageal dysmotility induced by bile. Other molecular path may play the role in this scenario.