The Respiratory-Heart Rate Interaction: Quantification and Physiological Mechanisms
Mccabe, Philip Michael
This item is only available for download by members of the University of Illinois community. Students, faculty, and staff at the U of I may log in with your NetID and password to view the item. If you are trying to access an Illinois-restricted dissertation or thesis, you can request a copy through your library's Inter-Library Loan office or purchase a copy directly from ProQuest.
Permalink
https://hdl.handle.net/2142/77629
Description
Title
The Respiratory-Heart Rate Interaction: Quantification and Physiological Mechanisms
Author(s)
Mccabe, Philip Michael
Issue Date
1982
Department of Study
Biology
Discipline
Biology
Degree Granting Institution
University of Illinois at Urbana-Champaign
Degree Name
Ph.D.
Degree Level
Dissertation
Keyword(s)
Biology, Animal Physiology
Language
eng
Abstract
This series of studies examines the respiratory-heart rate interaction and evaluates a measure of this phenomenon, generated through spectral analysis, as a non-invasive estimate of neural influences on the heart. The respiratory influence on heart rate, respiratory sinus arrhythmia (RSA), is a naturally occurring cardiac arrhythmia in which heart rate fluctuates with a periodicity similar to respiration. Studies of the physiological mechanisms of RSA suggest that the primary efferent neural contribution to RSA is via the vagus. In fact, it has been suggested that the relationship between RSA and vagal activity is so strong, that RSA may be used as a non-invasive estimate of parasympathetic control of the heart.
Traditionally, RSA has been quantified by measuring theamplitude of heart rate fluctuations around the mean heart rate.However, in freely behaving, unanesthetized subjects RSA is oftenmasked by other physiological influences on the heart. Therefore,spectral analysis, a time-series procedure, was used to partition thevarious influences on the heart by decomposing the heart periodvariance into its constituent frequencies. The heart period variabilitythat occurs at the respiratory frequencies was defined as V, an(' )estimate of RSA.
Since RSA has been reported to be related to vagal activity, it^was hypothesized that V would parallel changes in vagal control of(' )^the heart. Studies are presented which examine changes in V, in(' )^addition to other non-invasive estimates, heart period and heart^period variance, as a function of manipulations of neural tone to^the heart. Specifically, cardiac neural tone was manipulated by: (a) pharmacological manipulation of the baroreceptor reflex via injection or continuous infusion of phenylephrine or nitroprusside in rats and cats; and (b) electrical stimulation of barosensory fibers (aortic depressor nerve) in rabbits. In addition, the relative contributions of the sympathetic and parasympathetic nervous systems were examined following selective pharmacological blockade with beta-adrenergic blockers or atropine.
The synthesis of these studies suggests that in anesthetized andfreely behaving animals, across species, using different types ofneural tone manipulations, V is a robust, predictable estimate of(' )cardiac vagal tone. Moreover, V appears to be less influenced by(' )extra-vagal factors than other non-invasive cardiac measures, specifically heart period and heart period variance.
Use this login method if you
don't
have an
@illinois.edu
email address.
(Oops, I do have one)
IDEALS migrated to a new platform on June 23, 2022. If you created
your account prior to this date, you will have to reset your password
using the forgot-password link below.
