Mechanisms of Chemoreflex Control of Muscle Sympathetic Nerve Activity and Blood Pressure in Humans

dc.contributor.advisorSmith, Michael
dc.contributor.committeeMemberShi, Xiangrong
dc.contributor.committeeMemberClark, Michael
dc.creatorHardisty, Janelle M.
dc.date.accessioned2019-08-22T20:49:31Z
dc.date.available2019-08-22T20:49:31Z
dc.date.issued2004-05-01
dc.date.submitted2013-08-06T13:54:06-07:00
dc.description.abstractHardisty, Janelle M., Mechanisms of Chemoreflex Control of Muscle Sympathetic Nerve Activity and Blood Pressure in Humans. Doctor of Philosophy (Integrative Physiology), May 2004. The mechanisms linking obstructive sleep apnea (OSA) and cardiovascular disease are not fully understood; however, studies report patients with OSA exhibit chronic elevations in muscle sympathetic nerve activity (MSNA). This appears to be due to altered chemoreflex control of MSNA, mediated primarily by hypoxia. Yet, a correlation between degree of hypoxia and chemoreflex control of MSNA is unknown. Therefore, it was evaluated whether degree of hypoxia occurring during apnea determines the sympathoexcitatory and blood pressure responses, and whether these responses are augmented in OSA patients. Additionally, it was studied whether altered chemoreflex function in OSA patients is predictive of blood pressure response to apnea. In a clinical setting, the blood pressure response to voluntary apnea was determined to evaluate whether this could be used as a non-invasive measure of chemoreflex gain in OSA. Finally, the effect of hyperoxia on MSNA was studied to determine whether 15 min of hyperoxia, following intermittent hypoxic apnea, reverses the elevation of MSNA and altered chemoreflex control of MSNA. Consistent with the hypotheses, a relationship between MSNA responses, blood pressure response and level of hypoxia were determined. MSNA and peak systolic pressure responses were augmented in OSA subjects (p≤0.05 and p≤0.05, respectively), as well as, chemoreflex gain (p≤0.05). Clinically, peak systolic pressure responses to apnea were augmented in OSA patients (p˂0.001). Finally, basal MSNA and chemoreflex control of MSNA, following hyperoxia, was not different from baseline through 180 min of recovery (p=0.940 and p=0.278, respectively). These data support the hypotheses that chemoreflex gain is predicative of the blood pressure response; and furthermore, the MSNA and blood pressure responses to hypoxic apnea are augmented in OSA. Additionally, peak systolic pressure responses to voluntary apnea are augmented in OSA. Additionally, peak systolic pressure responses to voluntary apnea are augmented in OSA patients and could possibly be used as a marker of chemoreflex gain. Moreover, these data support the hypothesis that hyperoxia can reverse basal sympathoexcitation and augmented chemoreflex control of MSNA, associated with hypoxic apnea, supporting that elevations in MSNA are hypoxia mediated.
dc.format.mimetypeapplication/pdf
dc.identifier.urihttps://hdl.handle.net/20.500.12503/28813
dc.language.isoen
dc.provenance.legacyDownloads0
dc.subjectBehavioral Neurobiology
dc.subjectBehavior and Behavior Mechanisms
dc.subjectBehavior and Ethology
dc.subjectCardiovascular System
dc.subjectCirculatory and Respiratory Physiology
dc.subjectDiseases
dc.subjectLife Sciences
dc.subjectMedical Neurobiology
dc.subjectMedical Sciences
dc.subjectMedicine and Health Sciences
dc.subjectNervous System
dc.subjectNervous System Diseases
dc.subjectPhysiology
dc.subjectSystems and Integrative Physiology
dc.subjectSystems Neuroscience
dc.subjectChemoreflex control
dc.subjectmuscle sympathetic nerve activity
dc.subjectMSNA
dc.subjectblood pressure
dc.subjectobstructive sleep apnea
dc.subjecthypoxia
dc.subjectvoluntary apnea
dc.subjectbasal sympathoexcitation
dc.titleMechanisms of Chemoreflex Control of Muscle Sympathetic Nerve Activity and Blood Pressure in Humans
dc.typeDissertation
dc.type.materialtext
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.nameDoctor of Philosophy

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