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dc.contributor.authorNagy, Amy Daeen_US
dc.date.accessioned2014-03-14T21:38:54Z
dc.date.available2014-03-14T21:38:54Z
dc.date.issued2008-05-23en_US
dc.identifier.otheretd-06222008-193126en_US
dc.identifier.urihttp://hdl.handle.net/10919/43374
dc.description.abstractThis study was aimed at characterizing the apoptotic response equine small intestine subjected to experimental ischemia-reperfusion injury and determining if use of an angiotensin converting enzyme inhibitor (enalaprilat) would ameliorate the apoptotic response. It was designed to determine if mucosal epithelial cells undergo apoptosis during the ischemia phase and also examined if apoptosis is significantly exacerbated by reperfusion. It also investigated whether administration of enalaprilat decreased reperfusion injury secondary to reduced enterocyte apoptosis. Injury was induced using a low flow model of I-R. During celiotomy a single loop of jejunum was isolated and arterial flow decreased to 20% of baseline for one hour and complete occlusion for a second hour. Reperfusion was monitored for 3 hours. A control group (n=6) were not treated while the treatment group (n=6) received 0.5 mg/kg enalaprilat in 0.9% NaCl immediately following ischemia. Jejunal samples were taken prior to the induction of ischemia, immediately post-ischemia and at 1, 2 and 3 hours of reperfusion. Samples were evaluated for gross tissue pathology with standard hematoxylin and eosin staining, the presence of apoptotic cells via TUNEL staining, and gene expression of three apoptosis related genes (bax, bcl-2, p53) using qPCR. Serum enalaprilat and ACE concentrations were determined from blood samples drawn concurrent with jejunal sampling using HPLC/MS and standard HPLC. Plasma enalaprilat concentrations were comparable to previous reports in awake horses. Enalaprilat appeared to have no effect on serum ACE concentrations, however a significant spike in ACE concentration occurred in the treatment group at 1 hour of reperfusion (P=0.0001). Grade of mucosal damage was not significantly different between control and treatment groups at any time point. Subjectively apoptotic index appeared to be higher in the treatment group at end ischemia and during reperfusion. There were no changes in expression of p53 or bcl-2 in either group. Bax expression was significantly decreased (P= 0.02) in the control group at 2 hours of reperfusion. Based on our data administration of an ACE inhibitor during anesthesia in horses with an ischemic segment of intestine confers no protective benefit and may be associated with increased intestinal injury and apoptosis. Lack of expression of p53, bax and bcl-2 suggests another apoptotic mechanism in equine ischemic intestine.en_US
dc.publisherVirginia Techen_US
dc.relation.haspartThesisETD102808.pdfen_US
dc.relation.haspartNagyCopyrightPermissions.pdfen_US
dc.rightsI hereby certify that, if appropriate, I have obtained and attached hereto a written permission statement from the owner(s) of each third party copyrighted matter to be included in my thesis, dissertation, or project report, allowing distribution as specified below. I certify that the version I submitted is the same as that approved by my advisory committee. I hereby grant to Virginia Tech or its agents the non-exclusive license to archive and make accessible, under the conditions specified below, my thesis, dissertation, or project report in whole or in part in all forms of media, now or hereafter known. I retain all other ownership rights to the copyright of the thesis, dissertation or project report. I also retain the right to use in future works (such as articles or books) all or part of this thesis, dissertation, or project report.en_US
dc.subjectreperfusionen_US
dc.subjectischemiaen_US
dc.subjectapoptosisen_US
dc.subjectequineen_US
dc.titleApoptosis in the equine small intestine following experimental ischemia-reperfusion injuryen_US
dc.typeThesisen_US
dc.contributor.departmentLarge Animal Clinical Sciencesen_US
thesis.degree.nameMaster of Scienceen_US
thesis.degree.levelmastersen_US
thesis.degree.grantorVirginia Polytechnic Institute and State Universityen_US
dc.contributor.committeechairWhite, Nathaniel A. IIen_US
dc.contributor.committeememberMcCutcheon, L. Jillen_US
dc.contributor.committeememberBlikslager, Anthonyen_US
dc.contributor.committeememberTschetter, Jolynneen_US
dc.contributor.committeememberCrisman, Mark Virgilen_US
dc.identifier.sourceurlhttp://scholar.lib.vt.edu/theses/available/etd-06222008-193126/en_US
dc.date.sdate2008-06-22en_US
dc.date.rdate2008-11-05
dc.date.adate2008-11-05en_US


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