Determinants of respiratory sinus arrhythmia in the vagotomized
rabbit.
Perlini, Stefano, Pier Luigi Sold[acute]a, Massimo Piepoli, Giuseppe
Sala-Gallini, Alessandro Calciati, Giorgio Finardi, Luciano Bernardi.
Department of Internal Medicine, Clinica Medica 1, University of
Pavia, and Intensive Care Unit, IRCCS S.Matteo, Pavia, Italy
APStracts 2:0202H, 1995.
After cardiac denervation a small amplitude respiratory sinus
arrhythmia (RSA) has been described in animals and in man. Its
mechanical and chemical determinants were investigated in 19
urethane-anesthetized, vagotomized and mechanically-ventilated
rabbits. We measured the influence on RSA of arterial blood gases,
beta-adrenergic blockade, phasic and steady changes in right atrial
pressure (RAP) induced by changes in tidal volume (Vt: 20-40-60 ml),
respiratory frequency (RF: 10-20-30 cycles/minute) and dextran
-induced RAP increases, respectively. Phasic changes in RAP during
each recording were quantified as the standard deviation of the first
derivative of the RAP signal (dRAP), as a measure of the magnitude of
the variations of the rate of change due to respiration. RSA was
assessed by combined autoregressive power spectral analysis of R-R
interval and respiration on sequences of 256 heart beats. Despite
vagotomy, RSA was present in all recordings in all animals. While
breathing room air, RSA changes were dependent on both RF and Vt
(p<0.025 and p<0.001, respectively) and correlated with dRAP
(p<0.001) and with PaO2 (p<0.001). Beta-adrenergic blockade did
not change either the amplitude of this residual RSA or its
dependence on ventilatory mechanics. Dextran-induced increase in mean
RAP from 2.9 to 11.9 mmHg did not modify RSA nor dRAP. During 100% O2
inhalation, RSA changes were no longer significantly linked to RF and
Vt, and also the correlation of RSA with dRAP was reduced (p<0.05).
Changing the PaCO2 from 28 to 79 mmHg (induced by increasing the dead
space at fixed ventilation) did not modify RSA. Thus, after urethane
anesthesia and vagotomy RSA does persist and seems to be proportional
to changes in ventilation through phasic (rather than steady) changes
in RAP, presumably by the increase in mechanical stretch imposed on
the sinoatrial node by inspiratory increases in venous return. 100%
oxygen, but not raised PaCO2, consistently reduced these mechanically
induced changes in RSA, by a mechanism which is not known.
Received 14 April 1993; accepted in final form 18 April 1995.
APS Manuscript Number H328-3.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 26 May 1995.