PREDICTION OF TONIC PARASYMPATHETIC CARDIAC CONTROL USING RESPIRATORY SINUS ARRHYTHMIA - THE NEED FOR RESPIRATORY CONTROL
PREDICTION OF TONIC PARASYMPATHETIC CARDIAC CONTROL USING RESPIRATORY SINUS ARRHYTHMIA - THE NEED FOR RESPIRATORY CONTROL
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DOI：
10.1111/j.1469-8986.1991.tb00412.x
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发表时间：
1991-03-01
期刊：
影响因子：
3.7
通讯作者：
WIELING, W
中科院分区：
文献类型：
--
作者：
GROSSMAN, P;KAREMAKER, J;WIELING, W
呼吸性窦性心律失常（RSA）近年来受到广泛关注，因为大量证据表明这种现象的变化代表副交感神经心脏控制的改变。虽然呼吸性窦性心律失常似乎是由迷走神经机制介导的，但众所周知的呼吸影响（即速率和潮气量）对呼吸性窦性心律失常（改变其强度）的程度可能会调节RSA与心脏迷走神经张力之间的关系，这一点从未得到系统的研究。我们通过检查6名健康男性成人在静脉注射10毫克-肾上腺素受体阻滞剂心得安后RSA强度、呼吸（频率和潮气量）和心脏周期之间的个体关系来解决这一问题。受试者被暴露于各种行为任务中，这些任务改变了所有测量的生理变量。β阻断后心脏期的变化被认为主要是迷走神经介导的。受试者内回归分析一致显示，呼吸参数影响RSA强度，但不影响β -阻滞心脏期的强直性变化，这表明呼吸介导的RSA改变与心脏迷走神经张力的变化无关。只有当呼吸变量在统计上得到控制时，才有证据表明β -阻滞心期与RSA振幅之间存在合理的对应关系，这为将RSA振幅作为心脏迷走神经张力的指标时需要控制呼吸参数的观点提供了支持。重复测量的心期和呼吸性窦性心律失常平均水平的方差分析补充并支持了个体内的结果。这些发现表明，当使用呼吸性窦性心律失常作为心脏迷走神经指数时，控制呼吸参数的重要性。
Respiratory sinus arrhythmia (RSA) has received much attention in recent years due to the large body of evidence indicating that variations in this phenomenon represent alterations in parasympathetic cardiac control. Although it appears that respiratory sinus arrhythmia is mediated by vagal mechanisms, the extent to which the well-known respiratory influences (i.e., rate and tidal volume) on respiratory sinus arrhythmia (in altering its magnitude) may moderate the relationship between RSA and cardiac vagal tone has never been systematically studied.We addressed this issue by examining intraindividual relationships among RSA magnitude, respiration (rate and tidal volume), and heart period among six healthy male adults after intravenous administration of 10 mg propranolol, a beta-adrenergic blocker. Subjects were exposed to various behavioral tasks which altered all physiological variables measured. Variations in heart period after beta blockade were assumed to be predominantly vagally mediated. Within-subject regression analyses consistently showed that respiratory parameters influenced RSA magnitude, but not tonic variations in beta-blocked heart period, suggesting that respiratory-mediated RSA alterations are not associated with changes in cardiac vagal tone. Only when respiratory variables were statistically controlled was there evidence of a reasonable correspondence between beta-blocked heart period and RSA amplitude, providing support for the idea that respiratory parameters need to be controlled when using RSA amplitude as an index of cardiac vagal tone. Repeated-measures analyses of variance of mean levels of heart period and respiratory sinus arrhythmia across subjects supplemented and supported the intraindividual results. These findings point to the importance of controlling for respiratory parameters when using respiratory sinus arrhythmia as a cardiac vagal index.