Foram selecionados transversalmente 78 pacientes portadores de doença do refluxo gastroesofageano (DRGE) segundo critérios rigorosos de pHmetria esofageana ambulatorial de 24h (pHM-24h) e distribuídos em três grupos etários: Grupo A = 14 e = 24 anos, Grupo B = 25 e = 54 anos e Grupo C = 55 e = 64 anos. A pHM-24h foi realizada segundo a padronização de DeMeester e para diagnóstico da esofagite de refluxo utilizou-se classificação de Savary-Miller. Os grupos foram semelhantes em parâmetros da pHM-24h (p>0,05) cujas valores médios estavam acima da normalidade. A comparação entre grupos etários diferentes com parâmetros semelhantes de refluxo ácido não possibilitou qualquer inferência entre intensidade de refluxo ácido e grau de esofagite. Quando os mesmos pacientes foram subagrupados conforme profundidade da lesão epitelial e confrontados nos grupos etários, houve diferença significativa nas esofagites sem solução de continuidade epitelial. Os achados reforçam que a DRGE é uma doença crônica e sem resolução espontânea. As bases de diagnóstico e seguimento da DRGE não podem prescindir da defesa individual em detrimento da quantidade de ácido refluído, sendo ambos importantes.

The purpose of this study was to explore the relationship between the intensity of acid reflux and severity of esophageal tissue damage in a cross-sectional study of patients with gastroesophageal reflux disease (GERD). Seventy-eight patients with were selected in accordance with the strict 24-hour ambulatory esophageal pHmetry (24h-pHM) criteria and distributed into three age groups: Group A: 14 - 24 years of age. Group B: 25 - 54; and Group C: 55 - 64. The 24h-pHM was carried out in accordance with DeMeester standardization, and the Savary-Miller classification for the diagnosis of reflux esophagitis was used. The groups were similar in 24h-pHM parameters (p > 0.05), having above normal values. For the study group as a whole, there was no correlation between age group and intensity of acid reflux, and there was no correlation between intensity of acid reflux and severity of esophageal tissue damage. However, when the same patients were sub-grouped in accordance with the depth of their epithelial injury and then distributed into age groups, there was a significant difference in esophagitis without epithelial discontinuity. Younger patients had less epithelial damage than older patients. Additionally, although there was a significant progression from the least severe to the moderate stages of epithelial damage among the age groups, there was no apparent difference among the age groups in the distribution between the moderate stages and most severe stages. The findings support the conclusion that the protective response of individuals to acid reflux varies widely. Continued aggression by acid reflux appears to lead to the exhaustion of individual mechanisms of epithelial protection in some patients, but not others, regardless of age or duration of the disease. Therefore, the diagnosis and follow-up of GERD should include both measurements of the quantity of refluxed acid and an assessment of the damage to the esophageal epithelium.

Nesta revisão do sistema nervoso entérico, enfatiza-se o mecanismo da inibição não-adrenérgica e não-colinérgica na contratilidade do sistema digestório. Introduz-se a síntese e metabolismo do óxido nítrico com apresentação das sintases do óxido nítrico. Atualiza-se mostrando o óxido nítrico como neurotransmissor do mecanismo inibitório não-adrenérgico e não-colinérgico, demonstrando sua atividade na musculatura lisa gastrointestinal e possível mecanismo intracelular através da cGMP. Após atualização do mecanismo do peristaltismo e do complexo motor migratório, faz-se uma descrição do íleo adinâmico. Por fim, todo raciocínio apresentado condensa-se na fisiopatologia do íleo adinâmico.

The non-adrenergic and non-cholinergic (NANC) inhibition has an important role in the intrinsic control of enteric nervous system (ENS). The ENS is poor in the upper digestive tract (esophagus and stomach) and totally present in the intestine. Starling and Bayliss experiments demonstrated the intrinsic activity of ENS in 1899. Since then there are searching for neurotransmitters of NANC like VIP (Vasoactive Intestinal Polypeptide) and ATP (Adenosine Triphosphate). Recent works demonstrate nitric oxide as a neurotransmitter of NANC. The nitric oxide (NO) is a gaseous molecule produced from L- arginine, with less than ten seconds half-life. The enzymes involved in the synthesis of NO are the NO synthases (NOS): neuronal NOS or isoform I, inducible NOS or isoform II, and endothelial NOS or isoform III. The isoform I and III are constitutive, and the isoform 11 is inducible. The mechanisms involved in the induction of isoform III are TNFα (Tumor Necrosis Factora), IL-Iβ (Interleukin I-β), and bacteria lypopolyssacarides stimulus. The intestinal smooth muscle motility is mediated by NANC and one example of this is the migratory motor complex (MMC). The MMC can be modified by infusion of NO-like drugs and this modification is reversed by infusion of L-NAME (L-arginine analog) in experimental trials with animals. The NO causes relaxation and inhibition of peristalsis in the small intestine. The adynamic ileum is a very common situation for surgeons. In the adynamic ileum is observed the dysfunction of MMC. The adynamic ileum induced by infusion of endotoxins is reverted by use of NOS inhibitors.