کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6004469 | 1579540 | 2013 | 7 صفحه PDF | دانلود رایگان |
IntroductionIntestinal inflammation alters colonic afferent nerve sensitivity which may contribute to patients' perception of abdominal discomfort. We aimed to explore whether mast cells and the cyclooxygenase pathway are involved in altered afferent nerve sensitivity during colitis.MethodsC57Bl6 mice received 3% dextran-sulfate sodium (DSS) in drinking water for 7 days to induce colitis. Control animals received regular water. On day 8 inflammation was assessed in the proximal colon by morphology and histology. Extracellular afferent nerve discharge was recorded from the mesenteric nerve of a 2 cm colonic segment. Subgroups were treated in vitro with the mast cell stabilizer doxantrazole (10â 4 M) or the cyclooxygenase inhibitor naproxen (10â 5 M).ResultsDSS colitis resulted in morphological and histological signs of inflammation. At baseline, peak firing was 11 ± 2 imp sâ 1 in colitis segments and 5 ± 1 imp sâ 1 in uninflamed control segments (p < 0.05; mean ± SEM; each n = 6). In colitis segments, afferent nerve discharge to bradykinin (0.5 μM) was increased to 47 ± 7 compared to 23 ± 6 imp sâ 1 in recordings from non-inflamed control tissue (p < 0.05). Mechanosensitivity during luminal ramp distension (0-80 cm H2O) was increased reaching 24 ± 5 imp sâ 1 at 80 cm H2O during colitis compared to 14 ± 2 in non-inflamed controls (p < 0.05). Doxantrazole or naproxen reduced afferent discharge to bradykinin and luminal ramp distension in colitis segments to control levels.ConclusionIntestinal inflammation sensitizes mesenteric afferent nerve fibers to bradykinin and mechanical stimuli. The underlying mechanism responsible for this sensitization seems to involve mast cells and prostaglandins.
Journal: Autonomic Neuroscience - Volume 174, Issues 1â2, March 2013, Pages 47-53