A nyelőcső nyálkahártya mikrokeringési változásai akut kisérletes reflux alatt az epés komponens kóroki szerepe

Our aims were to examine microcirculation during experimental reflux esophagitis in dogs. We compared the effects of microcirculation of the mucosa to 3-hr exposure with acid, mixed acid and bile, we measured the changes in constitutive and inducible nitric oxide synthase activity (cNOS and iNOS). M...

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Bibliographic Details
Main Authors: Szentpáli Károly
Kaszaki József
Erős Gábor
Tiszlavicz László
Paszt Attila
Lázár György ifj
Balogh Ádám
Boros Mihály
Format: Article
Published: 2003
Series:MAGYAR SEBÉSZET 56 No. 2
mtmt:1321686
Online Access:http://publicatio.bibl.u-szeged.hu/18767
Description
Summary:Our aims were to examine microcirculation during experimental reflux esophagitis in dogs. We compared the effects of microcirculation of the mucosa to 3-hr exposure with acid, mixed acid and bile, we measured the changes in constitutive and inducible nitric oxide synthase activity (cNOS and iNOS). METHODS: The microcirculation of the upper esophagus was investigated by intravital videomicroscopy. The functional capillary density (FCD), relative vessel area (RVA) and red blood cell velocity (RBCV) were measured. Mucosal barrier integrity was examined by vascular and epithelial permeability indices. Myeloperoxidase (MPO) enzyme activity, cNOS, iNOS activities and microscopic damage were examined in biopsies. RESULTS: The vascular permeability index, the RBCV and the RVA increased significantly in the treated groups, the FCD significantly decreased after acid exposure. The MPO and iNOS activities were significantly elevated in all treated groups. The cNOS activity did not change after exposure to acid + bile or acid, but significantly decreased after sole bile treatment. Severe mucosal damage was observed after bile exposure. CONCLUSION: Bile induced characteristic microcirculatory changes during experimental reflux esophagitis. Tissue damage and leukocyte infiltration could be exacerbated by bile-induced cNOS inhibition.
Physical Description:61-67
ISSN:0025-0295