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dc.contributor.advisorH. Fred Downey
dc.creatorRyou, Myoung-Gwi
dc.date.accessioned2019-08-22T21:34:41Z
dc.date.available2019-08-22T21:34:41Z
dc.date.issued2007-05-01T00:00:00-07:00
dc.date.submitted2013-10-03T07:42:04-07:00
dc.identifier.urihttps://hdl.handle.net/20.500.12503/29435
dc.description.abstractRyou, Myoung-gwi. Hypoxia conditioning suppresses nitric oxide production upon myocardial reperfusion. Master of Science (Integrative Physiology), May 2007, 61pp, 2 tables, 9 figures. This study was conducted in mongrel dogs to test the hypothesis that 20 d normobaric intermittent hypoxic conditioning (IHC) evokes cardioprotective adaptations of the myocardial nitric oxide synthase (NOS) system. Specifically, the proposal that IHC suppresses myocardial NOS activity sufficiently to dampen the cytotoxic burst of NO formation upon reperfusion of ischemic myocardium was tested. Mongrel dogs were conditioned by a 20 d program of IHC (FIO2 9.5-10%; 5-10 min hypoxia/cycle, 5-8 cycles/d with intervening 4 min normoxia). On day 21, ventricular myocardium was sampled for measuring NOS activity (colorimetric assay) and endothelial NOS (eNOS) content (immunoblot). In separate experiments, myocardial nitrite (NO2) release, an stable product of NO oxidation, was measured at baseline and during reperfusion following 1 h occlusion of the left anterior descending coronary artery (LAD). Values in IHC dogs were compared with respective values in non-conditioned, control dogs. IHC lowered left and right ventricular NOS activity by 60%, from 100-115 to 40-45 mU/g protein (P [less than] 0.01), and decreased eNOS content by 30%. IHC dampened cumulative NO2 release during the first 5 min reperfusion from 32 ± 7 to 14 ± 2 μmol/g (P [less than] 0.05), but did not alter hyperemic LAD flow (15 ± 2 vs. 13 ± 2 ml/g). Attenuation of the NOS/NO system may contribute to IHC-induced protection of myocardium from ischemia-reperfusion injury.
dc.format.mimetypeapplication/pdf
dc.language.isoen
dc.subjectCardiovascular System
dc.subjectCirculatory and Respiratory Physiology
dc.subjectComparative and Laboratory Animal Medicine
dc.subjectExercise Physiology
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.subjectPhysiology
dc.subjectSystems and Integrative Physiology
dc.subjectIntermittent hypoxia conditioning
dc.subjectnitric oxide production
dc.subjectmyocardial reperfusion
dc.subjectmongrel dogs
dc.subjectmyocardial nitric oxide synthase
dc.subjectleft anterior descending coronary artery
dc.subjectventricular NOS activity
dc.titleHypoxic Conditioning Suppresses Cytotoxic Nitric Oxide Production Upon Myocardial Reperfusion
dc.typeThesis
thesis.degree.departmentGraduate School of Biomedical Sciences
thesis.degree.disciplineIntegrative Physiology
thesis.degree.grantorUniversity of North Texas Health Science Center at Fort Worth
thesis.degree.nameMaster of Science
dc.contributor.committeeMemberRong Ma
dc.contributor.committeeMemberRaghu Krishnamoorty
dc.type.materialtext
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