کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2023484 1542450 2006 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Effects of cholecystokinin-8 induced gastric dysmotility on bile regurgitation during stress and molecular mechanisms
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شیمی
پیش نمایش صفحه اول مقاله
Effects of cholecystokinin-8 induced gastric dysmotility on bile regurgitation during stress and molecular mechanisms
چکیده انگلیسی

ObjectiveTo illustrate the existence of bile regurgitation under stress condition, and explore the possible effects and related mechanism of changes of plasma cholecystokinin octapeptide (CCK-8) and intragastric pH on stress-induced bile regurgitation in rats.Methods(1) Changes in plasma CCK-8 and gastric bile concentration were respectively measured by using radioimmunoassay (RIA) method while simultaneously calculating gastric ulcer index (UI) and intragastric pH; (2) Each isolated gastric strips were suspended in a tissue chamber to record the contractile responses by polyphysiograph; (3) The responsiveness of gastric smooth muscle cells (SMCs) to sulfated cholecystokinin octapeptide (CCK-8S) were examined using fura-2-loaded microfluorimetric measurement of intracellular calcium concentration ([Ca2+]i); (4) The current of L-type calcium channels (ICaL) of SMCs were recorded by patch clamp techniques.Results(1) Compared with the normal control group, plasma CCK-8 and gastric bile concentration significantly increased during stress (p < 0.01) and both simultaneously reached the peak at the time point of 2 h after stress; UI and intragastric pH apparently increased (p < 0.01); (2) Significant changes to CCK-8S were found in the mean contractile amplitude and frequency of circular muscle (CM) and longitudinal muscle (LM) of gastric antrum and pylorus; (3) CCK-8S-evoked significant increase in [Ca2+]i (p < 0.01) could be suppressed by CCK-A receptor (CCK-AR) antagonist; whereas a small but significant increase was still elicited by CCK-8S under condition of the removal of extracellular calcium or by given nifidipine; (4) CCK-8S-intensified calcium current (ICaL) apparently inhibited by respective administration of nifidipine, Ca2+-ATPase inhibitors or calcium dependent chloride channel (ICl–Ca) blocker (p < 0.01).ConclusionGastric mucosal damage induced by bile regurgitation is closely connected with gastric antrum and pylorus dysmotility evoked by CCK-8 during the stress. CCK-8S-evoked [Ca2+]i increase in gastric antrum and pylorus SMC depends on the release of intracellular calcium stores which activates L-type voltage-dependent calcium channels (VDCC) through the activation of calcium dependent chloride channels.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Regulatory Peptides - Volume 136, Issues 1–3, 11 September 2006, Pages 64–71
نویسندگان
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