Analysis of Neural Contributions to Ultradian Oscillations of Blood Pressure and Heart Rate in Dogs
Broten, Theodore Paul
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https://hdl.handle.net/2142/71451
Description
Title
Analysis of Neural Contributions to Ultradian Oscillations of Blood Pressure and Heart Rate in Dogs
Author(s)
Broten, Theodore Paul
Issue Date
1987
Doctoral Committee Chair(s)
Zehr, John E.
Department of Study
Physiology and Biophysics
Discipline
Physiology
Degree Granting Institution
University of Illinois at Urbana-Champaign
Degree Name
Ph.D.
Degree Level
Dissertation
Keyword(s)
Biology, Animal Physiology
Abstract
A remarkably stable and accurate FM telemetry system was used to obtain long-term recordings of mean arterial pressure (MAP) and heart rate (HR) from unanesthetized, free-running dogs. These data were analyzed for their harmonic content by applying standard Fast Fourier Transform (FFT) time series analysis techniques. The FFT coefficients were used to calculate power spectral density functions from which the primary oscillatory frequency and the associated power of the primary frequency were determined. Initial studies revealed coherent ultradian oscillations of MAP and HR with a period between 1-2 hours (hr). These oscillations were found to be in phase. The significant decrease in power of these oscillations following the administration of clonidine, a centrally acting alpha$\sb2$ agonist, suggested that the central nervous system was involved in the genesis of these rhythms. Peripheral ganglionic blockade induced by hexamethonium bromide (10mg/kg/hr) significantly reduced the power of both MAP and HR oscillations, demonstrating the contribution of the autonomic efferent nerves. Atropine sulfate (2mg/hr) potentiated the power of both MAP and HR oscillations (P $<$ 0.06) suggesting that vagal efferent nerves are not mediating either HR or MAP oscillations, and may actually attenuate them. Metoprolol (200mg/day; b.i.d. for 5 days), a beta$\sb1$ antagonist, significantly decreased the power of HR and MAP oscillations. Prazosin (50ug/kg/hr), an alpha$\sb1$ antagonist, significantly decreased the power of MAP oscillations but increased the power of HR oscillations. These latter two series suggest that sympathetic innervation of both the vasculature and the heart are involved in expressing these rhythms.
The role of the arterial baroreflexes in modulating these rhythms was also examined. Data from carotid sinus denervation, cervical aortic denervation, and combined sino-cervical aortic denervation suggest that afferent input from the baroreceptors is not necessary for the genesis of these ultradian rhythms. The carotid sinus baroreflex alone significantly buffers the magnitude of the MAP oscillations but does not affect the HR oscillations. These data also suggest that there are two functional ultradian oscillators, one for HR and one for MAP.
Lastly, the existence of these ultradian rhythms as well as other fluctuations in MAP were shown to significantly affect sampling paradigms for the estimation of 24 hour MAP. Statistical parameters describing the accuracy of short-term measurements as estimators of 24 hour MAP were described.
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