Abstract
After cardiac denervation, a small-amplitude respiratory sinus arrhythmia (RSA) has been described in animals and humans. Its mechanical and chemical determinants were investigated in 19 urethan-anesthetized, vagotomized, and mechanically ventilated rabbits. We measured the influence on RSA of arterial blood gases, β-adrenergic blockade, and 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/min), and dextran-induced RAP increases. Phasic changes in RAP during each recording were quantified as standard deviation of the first derivative of the RAP signal (dRAP) as a measure of magnitude of 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 heartbeats. Despite vagotomy, RSA was present in all recordings in all animals. During room air breathing, RSA changes were dependent on RF and VT (P <0.025 and P <0.001, respectively) and correlated with dRAP (P <0.001) and arterial PO2 (P <0.001). β-Adrenergic blockade did not change 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 or 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 arterial PCO2 from 28 to 79 mmHg (induced by increasing dead space at fixed ventilation) did not modify RSA. Thus, after urethan anesthesia and vagotomy, RSA persists 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. One hundred percent O2, but not raised arterial PCO2, consistently reduced these mechanically induced changes in RSA by an unknown mechanism.
| Original language | English |
|---|---|
| Journal | American Journal of Physiology - Heart and Circulatory Physiology |
| Volume | 269 |
| Issue number | 3 38-3 |
| Publication status | Published - 1995 |
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Keywords
- heart rate variability
- power spectral analysis
ASJC Scopus subject areas
- Physiology
Cite this
Determinants of respiratory sinus arrhythmia in the vagotomized rabbit. / Perlini, S.; Solda, P. L.; Piepoli, M.; Sala-Gallini, G.; Calciati, A.; Finardi, G.; Bernardi, L.
In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 269, No. 3 38-3, 1995.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Determinants of respiratory sinus arrhythmia in the vagotomized rabbit
AU - Perlini, S.
AU - Solda, P. L.
AU - Piepoli, M.
AU - Sala-Gallini, G.
AU - Calciati, A.
AU - Finardi, G.
AU - Bernardi, L.
PY - 1995
Y1 - 1995
N2 - After cardiac denervation, a small-amplitude respiratory sinus arrhythmia (RSA) has been described in animals and humans. Its mechanical and chemical determinants were investigated in 19 urethan-anesthetized, vagotomized, and mechanically ventilated rabbits. We measured the influence on RSA of arterial blood gases, β-adrenergic blockade, and 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/min), and dextran-induced RAP increases. Phasic changes in RAP during each recording were quantified as standard deviation of the first derivative of the RAP signal (dRAP) as a measure of magnitude of 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 heartbeats. Despite vagotomy, RSA was present in all recordings in all animals. During room air breathing, RSA changes were dependent on RF and VT (P <0.025 and P <0.001, respectively) and correlated with dRAP (P <0.001) and arterial PO2 (P <0.001). β-Adrenergic blockade did not change 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 or 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 arterial PCO2 from 28 to 79 mmHg (induced by increasing dead space at fixed ventilation) did not modify RSA. Thus, after urethan anesthesia and vagotomy, RSA persists 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. One hundred percent O2, but not raised arterial PCO2, consistently reduced these mechanically induced changes in RSA by an unknown mechanism.
AB - After cardiac denervation, a small-amplitude respiratory sinus arrhythmia (RSA) has been described in animals and humans. Its mechanical and chemical determinants were investigated in 19 urethan-anesthetized, vagotomized, and mechanically ventilated rabbits. We measured the influence on RSA of arterial blood gases, β-adrenergic blockade, and 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/min), and dextran-induced RAP increases. Phasic changes in RAP during each recording were quantified as standard deviation of the first derivative of the RAP signal (dRAP) as a measure of magnitude of 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 heartbeats. Despite vagotomy, RSA was present in all recordings in all animals. During room air breathing, RSA changes were dependent on RF and VT (P <0.025 and P <0.001, respectively) and correlated with dRAP (P <0.001) and arterial PO2 (P <0.001). β-Adrenergic blockade did not change 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 or 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 arterial PCO2 from 28 to 79 mmHg (induced by increasing dead space at fixed ventilation) did not modify RSA. Thus, after urethan anesthesia and vagotomy, RSA persists 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. One hundred percent O2, but not raised arterial PCO2, consistently reduced these mechanically induced changes in RSA by an unknown mechanism.
KW - heart rate variability
KW - power spectral analysis
UR - http://www.scopus.com/inward/record.url?scp=0029096319&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0029096319&partnerID=8YFLogxK
M3 - Article
C2 - 7573534
AN - SCOPUS:0029096319
VL - 269
JO - American Journal of Physiology
JF - American Journal of Physiology
SN - 0363-6119
IS - 3 38-3
ER -