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dc.contributor.advisorKorthuis, Ronald J.eng
dc.contributor.authorDai, Hongyaneng
dc.date.issued2011eng
dc.date.submitted2011 Summereng
dc.descriptionTitle from PDF of title page (University of Missouri--Columbia, viewed on May 18, 2012).eng
dc.descriptionThe entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file.eng
dc.descriptionIncludes bibliographical references.eng
dc.descriptionVita.eng
dc.descriptionDissertation advisor: Dr. Ronald Korthuiseng
dc.description"July 2011"eng
dc.description.abstract[ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT REQUEST OF AUTHOR.] Tissue ischemia occurs in patients with myocardial infarction, stroke and other vascular occlusive diseases. While restitution of blood supply is necessary to prevent the progression of tissue injury, it also initiates a complex series of microvascular inflammatory changes which paradoxically induce additional cellular damage beyond ischemia alone. Pharmacological preconditioning is a powerful protective intervention against ischemia and reperfusion (I/R) injury. Previous work from our laboratory demonstrated that treatment with the calcium activated, large conductance potassium (BKCa) channel opener NS-1619 24 hours prior to the induction of I/R in mice confers protection against intestinal I/R injury. The aims of the studies outlined in this dissertation thus were to examine the mechanisms underlying NS-1619-induced protection against oxidative injury in mice, rats and human microvascular endothelial cells (HMECs). Evidence presented in this dissertation supported the notions that: 1) NS-1619 elicits preconditioning against mice intestinal I/R injury in a reactive oxygen species (ROS) and heme oxygenase (HO)-1 dependent pathway; 2) the preconditioning induced by NS-1619 against oxidative injury in HMECs is independent of BKCa channel activation, but dependent upon ROS and HO-1; 3) connective tissue mast cells and proteases, especially matrix metalloproteinase-9 (MMP-9), contribute to the pathogenesis of arteriolar endothelium-dependent vasodilation dysfunction during intestinal I/R in rat mesentery.eng
dc.format.extentxii, 178 pageseng
dc.identifier.merlinb87210678eng
dc.identifier.oclc805707963eng
dc.identifier.urihttps://doi.org/10.32469/10355/14250eng
dc.identifier.urihttps://hdl.handle.net/10355/14250
dc.languageEnglisheng
dc.publisherUniversity of Missouri--Columbiaeng
dc.relation.ispartofcommunityUniversity of Missouri--Columbia. Graduate School. Theses and Dissertationseng
dc.rightsAccess is limited to the campuses of the University of Missouri.eng
dc.subjectischemiaeng
dc.subjectBK channeleng
dc.subjectreperfusioneng
dc.subjectpreconditioningeng
dc.subject.meshIschemia -- prevention & controleng
dc.subject.meshReperfusion Injury -- prevention & controleng
dc.subject.meshBenzimidazoles -- pharmacokineticseng
dc.subject.meshEndothelial Cells -- drug effectseng
dc.subject.meshIschemic Preconditioning -- methodseng
dc.subject.meshLarge Conductance Calcium Activated Potassium Channels -- metabolismeng
dc.subject.meshMesenteric Arteries -- drug effectseng
dc.subject.meshMesenteric Veins -- drug effectseng
dc.subject.meshOxidative Stress -- physiologyeng
dc.subject.meshReactive Oxygen Species -- metabolismeng
dc.titleMechanisms of BKCa channel agonist NS-1619-elicited protection against oxidative stress from venules to arterioleseng
dc.typeThesiseng
thesis.degree.disciplinePhysiology (Medicine) (MU)eng
thesis.degree.grantorUniversity of Missouri--Columbiaeng
thesis.degree.levelDoctoraleng
thesis.degree.namePh. D.eng


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