کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
4303080 1288470 2010 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Evaluating the Potential Role of Nitric Oxide as a Mediator of Hydrostatic Edema Mediated Intestinal Contractile Dysfunction
موضوعات مرتبط
علوم پزشکی و سلامت پزشکی و دندانپزشکی عمل جراحی
پیش نمایش صفحه اول مقاله
Evaluating the Potential Role of Nitric Oxide as a Mediator of Hydrostatic Edema Mediated Intestinal Contractile Dysfunction
چکیده انگلیسی

BackgroundAdministration of L-nil, a selective inhibitor of inducible nitric oxide synthase (iNOS), improves ileus in an animal model of resuscitation induced intestinal edema. The purpose of this study was to elucidate the iNOS/nitric oxide (NO) signal transduction pathway in intestinal edema.Materials and MethodsMale Sprague Dawley rats were divided into two groups; CONTROL and RESUS+VH (edema, 80 cc/kg normal saline (resuscitation) with mesenteric venous hypertension). iNOS mRNA and protein, iNOS activity, NO tissue levels, soluble guanylyl cyclase (sGC) expression, and cyclic guanosine monophosphate (cGMP) levels were measured. As a functional endpoint, we evaluated intestinal contractile strength and frequency in L-nil treated animals.ResultsEdema was associated with increased iNOS mRNA and protein expression without subsequent increases in iNOS activity or tissue NO levels. There was no significant change in sGC expression or increase in cGMP induced by edema. Administration of L-nil did not decrease edema development or preserve contractile strength, but increased contractile frequency.ConclusionHydrostatic intestinal edema is not associated with increased iNOS activity or tissue NO levels. Administration of L-nil in edema increases intestinal contractile frequency. This may represent a potential mechanism for the amelioration of ileus seen with the administration of L-nil.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Surgical Research - Volume 163, Issue 1, September 2010, Pages 102–109
نویسندگان
, , , , , , , , , , , ,