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dc.contributor.authorMyers, Christopheren_US
dc.contributor.authorCohen, Michaelen_US
dc.contributor.authorEckberg, Dwainen_US
dc.contributor.authorTaylor, J. Andrewen_US
dc.date.accessioned2011-11-14T19:02:50Z
dc.date.available2011-11-14T19:02:50Z
dc.date.issued2001-04
dc.identifier.urihttps://hdl.handle.net/2144/2281
dc.description.abstractBoth theoretic models and cross-spectral analyses suggest that an oscillating sympathetic nervous outflow generates the low frequency arterial pressure fluctuations termed Mayer waves. Fluctuations in heart rate also have been suggested to relate closely to Mayer waves, but empiric models have not assessed the joint causative influences of hemt rate and sympathetic activity. Therefore, we constructed a model based simply upon the hemodynamic equation deriving from Ohm's Law. With this model, we determined time relations and relative contributions of heart rate and sympathetic activity to the genesis of arterial pressure Mayer waves. We assessed data from eight healthy young volunteers in the basal state and in a high sympathetic state known to produce concurrent increases in sympathetic nervous outflow and Mayer wave amplitude. We fit the Mayer waves (0.05-0.20 Hz) in mean arterial pressure by the weighted sum ofleading oscillations in heart rate and sympathetic nerve activity. This model of our data showed heart rate oscillations leading by 2-3.75 seconds were responsible for almost half of the variance in arterial pressure (basal R^2=0.435±0.140, high sympathetic R^2=0.438±0.180). Surprisingly, sympathetic activity (lead 0-5 seconds) contributed only modestly to the explained variance in Mayer waves during either sympathetic state (basal: ∆R^2=0.046±0.026; heightened: ∆R^2=0.085±0.036). Thus, it appears that heart rate oscillations contribute to Mayer waves in a simple linear fashion, whereas sympathetic fluctuations contribute little to Mayer waves in this way. Although these results do not exclude an important vascular sympathetic role, they do suggest that additional Ji1ctors, such as sympathetic transduction into vascular resistance, modulate its influence.en_US
dc.description.sponsorshipBinda and Fred Shuman Foundation; National Institute on Aging (AG14376).en_US
dc.language.isoen_US
dc.publisherBoston University Computer Science Departmenten_US
dc.relation.ispartofseriesBU CAS/CNS Technical Reports;CAS/CNS-TR-2001-005
dc.rightsCopyright 2001 Boston University. Permission to copy without fee all or part of this material is granted provided that: 1. The copies are not made or distributed for direct commercial advantage; 2. the report title, author, document number, and release date appear, and notice is given that copying is by permission of BOSTON UNIVERSITY TRUSTEES. To copy otherwise, or to republish, requires a fee and / or special permission.en_US
dc.subjectHemodynamicsen_US
dc.subjectSpectral analysisen_US
dc.subjectHydraulic Resistance Equationen_US
dc.titleA Model for the Genesis of Arterial Pressure Mayer Waves from Heart Rate and Sympathetic Activityen_US
dc.typeTechnical Reporten_US
dc.rights.holderBoston University Trusteesen_US


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