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dc.contributor.authorSperou, Arissa
dc.contributor.otherQueen's University (Kingston, Ont.). Theses (Queen's University (Kingston, Ont.))en
dc.date2013-07-05 12:20:10.976en
dc.date2013-07-05 14:37:05.15en
dc.date.accessioned2013-07-05T18:57:40Z
dc.date.issued2013-07-05
dc.identifier.urihttp://hdl.handle.net/1974/8105
dc.descriptionThesis (Master, Anatomy & Cell Biology) -- Queen's University, 2013-07-05 14:37:05.15en
dc.description.abstractDeficient trophoblast invasion and spiral artery remodeling are associated with pregnancy complications such as pre-eclampsia (PE) and fetal growth restriction (FGR). Using a model in which pregnant Wistar rats are given daily, low-dose, injections of bacterial lipopolysaccharide (LPS; 10 – 40 µg/kg) on gestational days (GD) 13.5 – 16.5, our group has shown that abnormal maternal inflammation is causally linked to shallow trophoblast invasion, deficient spiral artery remodeling, and altered utero-placental hemodynamics leading to FGR/PE; these alterations were shown to be mediated by TNF-a. The present research evaluated certain consequences of decreased placental perfusion; this was accomplished by examining placental alterations indicative of decreased placental perfusion. Additionally, the role of glyceryl trinitrate (GTN) was determined as a potential therapeutic to prevent the consequences of decreased placental perfusion. Results indicated that dams experiencing heightened maternal inflammation showed significantly greater expression of hypoxia-inducible factor-1a (HIF-1a) and nitrotyrosine, both of which are markers of decreased perfusion and oxidative/nitrosative stress. Contrary to expectations, inflammation did not appear to affect nitric oxide (NO) bioavailability, as revealed by a lack of change in placental or plasma levels of cyclic guanosine monophosphate (cGMP). However, continuous transdermal administration of GTN (25 µg/hr) on GD 12.5 – 16.5 prevented the accumulation of HIF-1a and nitrotyrosine in placentas from LPS-treated rats. These results support the concept that maternal inflammation contributes to placental hypoxia and oxidative/nitrosative stress. Additionally, they indicate that GTN has potential applications in the treatment and/or prevention of pregnancy complications associated with abnormal maternal inflammation.en_US
dc.languageenen
dc.language.isoenen_US
dc.relation.ispartofseriesCanadian thesesen
dc.rightsThis publication is made available by the authority of the copyright owner solely for the purpose of private study and research and may not be copied or reproduced except as permitted by the copyright laws without written authority from the copyright owner.en
dc.subjectPregnancy Complicationsen_US
dc.subjectMaternal Inflammationen_US
dc.titleHeightened maternal inflammation is linked to placental oxidative and nitrosative stress associated with fetal growth restriction in the raten_US
dc.typethesisen_US
dc.description.restricted-thesisWe are currently working on a research paper using data presented in this thesis. We would like to keep the thesis restricted until the paper is published.en
dc.description.degreeMasteren
dc.contributor.supervisorGraham, Charles H.en
dc.contributor.departmentAnatomy and Cell Biologyen
dc.embargo.terms1825en
dc.embargo.liftdate2018-07-04


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