DETERMINANTS OF RESPIRATORY SINUS ARRHYTHMIA IN THE VAGOTOMIZED RABBIT

被引:35
作者
PERLINI, S
SOLDA, PL
PIEPOLI, M
SALAGALLINI, G
CALCIATI, A
FINARDI, G
BERNARDI, L
机构
[1] UNIV PAVIA, MED CLIN 1, DEPT INTERNAL MED, I-27100 PAVIA, ITALY
[2] IST RICOVERO & CURA CARATTERE SCI S MATTEO, INTENS CARE UNIT, I-27100 PAVIA, ITALY
来源
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY | 1995年 / 269卷 / 03期
关键词
POWER SPECTRAL ANALYSIS; HEART RATE VARIABILITY;
D O I
10.1152/ajpheart.1995.269.3.H909
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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, beta-adrenergic blockade, and phasic and steady changes in right atrial pressure (RAP) induced by changes in tidal volume (VT, 20, 40, 60 mi), 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). beta-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% O-2 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 O-2, but not raised arterial PCO2, consistently reduced these mechanically induced changes in RSA by an unknown mechanism.
引用
收藏
页码:H909 / H915
页数:7
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