The participatinn of the nitrergic pathway in icreased rate of transitory relaaxation of lower esophageal sphincter induced by rectal distension in dogs / A participação da via nitrérgica no aumento da taxa de relaxamento transitório do esfíncter esofágico inferior induzida pela distensão retal em cães

Context The rectal distension in dogs increases the rate of transitory lower esophageal sphincter relaxation considered the main factor causing gastroesophageal reflux. Objectives The aim of this study was evaluate the participation of the nitrergic pathway in the increased transitory lower esophageal sphincter relaxation rate induced by rectal distension in anesthetized dogs. Methods Male mongrel dogs (n = 21), weighing 10-15 kg, were fasted for 12 hours, with water ad libitum. Thereafter, they were anesthetized (ketamine 10 mg.Kg-1 + xylazine 20 mg.Kg-1), so as to carry out the esophageal motility evaluation protocol during 120 min. After a 30-minute basal period, the animals were randomly intravenous treated whith: saline solution 0.15M (1ml.Kg-1), L-NAME (3 mg.Kg-1), L-NAME (3 mg.Kg-1) + L-Arginine (200 mg.Kg-1), glibenclamide (1 mg.Kg-1) or methylene blue (3 mg.Kg-1). Forty-five min after these pre-treatments, the rectum was distended (rectal distension, 5 mL.Kg-1) or not (control) with a latex balloon, with changes in the esophageal motility recorded over 45 min. Data were analyzed using ANOVA followed by Student Newman-Keuls test. Results In comparison to the respective control group, rectal distension induces an increase in transitory lower esophageal sphincter relaxation. Pre-treatment with L-NAME or methylene blue prevents (P<0.05) this phenomenon, which is reversible by L-Arginine plus L-NAME. However, pretreating with glibenclamide failed to abolish this process. Conclusions Therefore, these experiments suggested, that rectal distension increases transitory lower esophageal sphincter relaxation in dogs via through nitrergic pathways. .

Contexto A distensão retal aumenta a taxa de relaxamento transitório do esfíncter esofágico inferior em cães, sendo o relaxamento transitório do esfíncter esofágico inferior considerado o principal fator responsável pelo refluxo gastroesofágico. Objetivos Avaliar a participação da via nitrérgica no aumento da taxa relaxamento transitório do esfíncter esofágico inferior induzida por distensão retal em cães anestesiados. Métodos Cães sem raça definida, machos (n = 21), pesando entre 10-15 kg, foram mantidos em jejum durante 12 horas, no entanto, com água ad libitum. Depois disso, eles foram anestesiados (cetamina 10 mg.Kg-1 + xilazina 20 mg.Kg-1), para a realização do protocolo de avaliação da motilidade esofágica durante 120 minutos. Após um período basal de 30 minutos, os animais foram aleatoriamente tratados intravenosa com: solução salina 0,15 (1 ml.Kg-1), L-NAME (3 mg.Kg-1), L-NAME (3 mg.Kg-1) + L-arginina (200 mg.Kg-1), glibenclamida (1 mg.Kg-1) e azul de metileno (3 mg.Kg-1). Quarenta e cinco minutos após os pré-tratamentos, o reto foi distendido com um balão de látex (DR, 5 mg.Kg-1) ou não (grupo controle), e as variações da motilidade esofágica foram registradas e gravadas ao longo dos 45 minutos seguintes. Os dados foram analisados utilizando-se ANOVA seguido pelo teste de Student Newman-Keuls. Resultados Em comparação com o respectivo grupo controle, a distensão retal demonstrou induzir um aumento na taxa de relaxamento transitório do esfíncter esofágico inferior. O pré-tratamento com L -NAME ou azul de metileno impediu (P<0,05) este fenômeno, que foi reversível após a administração de L-Arginina + L-NAME. No entanto, o pré-tratamento com a glibenclamida não ...

Alteration of nitrergic neuromuscular transmission as a result of acute experimental colitis in rat

Nitric oxide (NO) is a non-adrenergic, non-cholinergic neurotransmitter found in the enteric nervous system that plays a role in a variety of enteropathies, including inflammatory bowel disease. Alteration of nitrergic neurons has been reported to be dependent on the manner by which inflammation is caused. However, this observed alteration has not been reported with acetic acid-induced colitis. Therefore, the purpose of the current study was to investigate changes in nitrergic neuromuscular transmission in experimental colitis in a rat model. Distal colitis was induced by intracolonic administration of 4% acetic acid in the rat. Animals were sacrificed at 4 h and 48 h postacetic acid treatment. Myeloperoxidase activity was significantly increased in the acetic acid-treated groups. However, the response to 60 mM KCl was not significantly different in the three groups studied. The amplitude of phasic contractions was increased by Nomega-nitro-L-arginine methyl ester (L-NAME) in the normal control group, but not in the acetic acid-treated groups. Spontaneous contractions disappeared during electrical field stimulation (EFS) in normal group. However, for the colitis groups, these contractions initially disappeared, and then reappeared during EFS. Moreover, the observed disappearance was diminished by L-NAME; this suggests that these responses were NO-mediated. In addition, the number of NADPH-diaphorase positive nerve cell bodies, in the myenteric plexus, was not altered in the distal colon; whereas the area of NADPH-diaphorase positive fibers, in the circular muscle layer, was decreased in the acetic acidtreated groups. These results suggest that NO-mediated inhibitory neural input, to the circular muscle, was decreased in the acetic acid-treated groups.