Mechanisms of Post-Apneic Symathoinhibition in Humans

dc.contributor.advisorMichael Smith
dc.contributor.committeeMemberDavid Barker
dc.contributor.committeeMemberJohn R Burk
dc.creatorSwift, Nicolette Muenter
dc.description.abstractMuenter Swift, Nicolette, Mechanisms of Post-Apneic Sympathoinhibition in Humans. Doctor of Philosophy (Biomedical Sciences), August, 2002, 110 pp., 14 figures, references. Apnea is accompanied by a concomitant rise in arterial pressure and muscle sympathetic nerve activity (MSNA), the latter primarily due to chemoreflex stimulation and possibly the lack of sympathoinhibitory input from pulmonary stretch receptors. The progressive sympathoexcitation during apnea suggests a possible overriding of arterial baroreflex sympathoinhibitory input to sympathoregulatory centers by apnea-induced sympathoexcitatory mechanisms. Nevertheless, it is unknown whether apnea attenuates baroreflex control of MSNA. Apnea termination is accompanied by a profound and immediate sympathoinhibition, the mechanisms of which are unclear; however, potential mediators include normalization of blood gases (i.e. chemoreflex unloading), the lung inflation reflex, and arterial baroreflex stimulation. Therefore, the purpose of the current studies was to: i) determine the contribution of chemoreflex unloading to post-apneic sympathoinhibition, ii) determine the contribution of the lung inflation reflex to post-apneic sympathoinhibition, and iii) determine whether carotid baroreflex control of MSNA is altered by apnea and its termination. The first study compared MSNA during post-apneic administration of room air versus a gas mixture designed to maintain the subjects’ end-apneic alveolar gas levels. Regardless of post-apneic gas administration, post-apneic MSNA was at or below baseline pre-apneic levels; thus; chemoreflex unloading does not contribute to post-apneic sympathoinhibition. Furthermore, quantification of post-apneic MSNA associated only with the low lung volume phase of respiration, when sympathoinhibitory input from the lung inflation reflex is minimal, demonstrated that post-apneic sympathoinhibition persists even during the low lung volume phase of respiration, when sympathoinhibitory input from the lung inflation reflex is minimal, demonstrated that post-apneic sympathoinhibition persists even during the low lung volume phase of respiration. Therefore, the lung inflation reflex does not appear to be the primary mediator of post-apneic sympathoinhibition. The second study utilized neck suction (NS) and neck pressure (NP) to assess carotid baroreflex function during and following sleep apnea. The sympathoinhibitory response to -60 Torr NS was maintained throughout apnea; conversely, the sympathoexcitatory response to +30 Torr NP was attenuated for nearly one minute post-apnea. Thus, carotid baroreflex control of MSNA is not altered by apnea but is transiently attenuated by apnea termination. We propose that the carotid baroreflex-MSNA function curve resets rightward and upward during apnea. Return of the function curve to baseline upon apnea termination may partly explain the reduced MSNA response to NP post-apnea.
dc.subjectBehavior and Behavior Mechanisms
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.subjectMotor Control
dc.subjectNervous System
dc.subjectNervous System Diseases
dc.subjectRespiratory System
dc.subjectRespiratory Tract Diseases
dc.subjectPost-apneic sympathoinhibition
dc.subjectsleep apnea
dc.subjectarterial pressure
dc.subjectmuscle sympathetic nerve activity
dc.subjectchemoreflex stimulation
dc.subjectpulmonary stretch receptors
dc.subjectcarotid baroreflex control
dc.subjectlung inflation reflex
dc.titleMechanisms of Post-Apneic Symathoinhibition in Humans
dc.type.materialtext School of Biomedical Sciences Sciences of North Texas Health Science Center at Fort Worth of Philosophy


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