Effects of intermittent hypoxia on cardiovascular and cerebrovascular function: implications for obstructive sleep apnoea
dc.contributor.advisor | Poulin, Marc J. | |
dc.contributor.advisor | Hanly, Patrick J. | |
dc.contributor.author | Foster, Glen Edward | |
dc.date.accessioned | 2017-12-18T21:57:23Z | |
dc.date.available | 2017-12-18T21:57:23Z | |
dc.date.issued | 2009 | |
dc.description | Bibliography: p. 137-151 | en |
dc.description.abstract | Intermittent hypoxia is thought to be an important contributor to the increased risk of cardiovascular and cerebrovascular disease observed in patients with obstructive sleep apnoea (OSA). This thesis reports findings from three major experiments designed to examine the relationship between OSA, intermittent hypoxia, and vascular function. In Study 1, the cerebral vascular response to hypoxia was assessed in newly diagnosed patients with OSA, both before and after 4-6 weeks of continuous positive airway pressure (CP AP). The cerebral blood flow response to hypoxia was found to be significantly reduced in patients with OSA and treatment with CPAP normalized this response. An attenuated cerebral blood flow response to hypoxia may contribute to an increased risk for cerebral vascular disease. In Study 2, the cardiovascular and cerebrovascular responses to acute hypoxia were assessed following exposure to prolonged bouts of intermittent hypoxia in healthy human subjects. The results from this study demonstrate that intennittent hypoxia can enhance the presser response to hypoxia and increase resting arterial pressure. Furthermore, the cerebral vascular response to hypoxia and the production of nitric oxide were reduced with intermittent hypoxia. These findings suggest that intennittent hypoxia affects blood pressure and cerebrovascular regulation which is, therefore, likely to contribute to the pathogenesis of cardiovascular and cerebrovascular disease in OSA patients. Study 3 was designed to assess the importance of the angiotensin-II type-I receptor in the cardiovascular response to a single six-hour bout of intermittent hypoxia. Healthy human subjects took part in a double blind, placebo-controlled, and randomized, crossover study. The results demonstrate the importance of the type-I angiotensin-II receptor in mediating the hypertensive response associated with intennittent hypoxia. Taken together, the results from these three studies provide evidence to support the hypothesis that intermittent hypoxia exposure similar to that experienced by OSA patients can contribute to changes in cardiovascular and cerebrovascular regulation. Ultimately, these regulatory changes may be precursors to the development of cardiovascular and cerebrovascular disease in OSA. | |
dc.format.extent | 162 leaves : ill. ; 30 cm. | en |
dc.identifier.citation | Foster, G. E. (2009). Effects of intermittent hypoxia on cardiovascular and cerebrovascular function: implications for obstructive sleep apnoea (Doctoral thesis, University of Calgary, Calgary, Canada). Retrieved from https://prism.ucalgary.ca. doi:10.11575/PRISM/2978 | en_US |
dc.identifier.doi | http://dx.doi.org/10.11575/PRISM/2978 | |
dc.identifier.uri | http://hdl.handle.net/1880/103979 | |
dc.language.iso | eng | |
dc.publisher.institution | University of Calgary | en |
dc.publisher.place | Calgary | en |
dc.rights | University of Calgary graduate students retain copyright ownership and moral rights for their thesis. You may use this material in any way that is permitted by the Copyright Act or through licensing that has been assigned to the document. For uses that are not allowable under copyright legislation or licensing, you are required to seek permission. | |
dc.title | Effects of intermittent hypoxia on cardiovascular and cerebrovascular function: implications for obstructive sleep apnoea | |
dc.type | doctoral thesis | |
thesis.degree.discipline | Cardiovascular & Respiratory Sciences | |
thesis.degree.grantor | University of Calgary | |
thesis.degree.name | Doctor of Philosophy (PhD) | |
ucalgary.item.requestcopy | true | |
ucalgary.thesis.accession | Theses Collection 58.002:Box 1859 520502029 | |
ucalgary.thesis.notes | UARC | en |
ucalgary.thesis.uarcrelease | y | en |
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