TRANSFER-FUNCTION ANALYSIS OF THE CIRCULATION - UNIQUE INSIGHTS INTO CARDIOVASCULAR REGULATION
TRANSFER-FUNCTION ANALYSIS OF THE CIRCULATION - UNIQUE INSIGHTS INTO CARDIOVASCULAR REGULATION
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DOI：
10.1152/ajpheart.1991.261.4.h1231
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发表时间：
1991-10-01
影响因子：
--
通讯作者：
COHEN, RJ
中科院分区：
文献类型：
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作者：
SAUL, JP;BERGER, RD;COHEN, RJ
我们以前已经证明，传递函数分析可以用来精确地表征正常人的呼吸性窦性心律失常(RSA)。为了进一步研究自主神经系统在RSA中的作用，并了解呼吸活动和动脉压之间的复杂联系，我们测定了14名健康受试者在以预定但不稳定的方式控制呼吸频率的6分钟时间内，呼吸、心率(HR)与时相、收缩压、舒张压和脉压之间的传递函数。阿托品、心得安及两者的药理自主神经阻断，结合体位的改变，被用来表征交感神经和迷走神经对这些关系的贡献，并从RSA对动脉压的影响中剖析呼吸和动脉压之间的直接机械联系。我们发现：(1)纯交感(立位+阿托品)HR反应在>；0.1赫兹处幅度显著降低，且有一个相位延迟，而单纯迷走神经(仰卧+心得安)对HR的调制在所有频率上都具有较高幅度且无相位延迟的特点；2)呼吸与动脉压之间的机械联系和RSA对呼吸对动脉压的影响均有显著贡献；3)RSA对动脉压波动的贡献对迷走神经作用显著，对交感神经调节作用不显著；4)呼吸对动脉压的机械作用与瞬时肺容量的负变率有关；5)收缩时的机械效应大于舒张期的机械效应；6)站立时的机械效应大于仰卧位。这些发现中的大多数可以用一个简单的循环控制模型来解释，该模型基于我们实验室以前发表的实验传递函数。
We have demonstrated previously that transfer function analysis can be used to precisely characterize the respiratory sinus arrhythmia (RSA) in normal humans. To further investigate the role of the autonomic nervous system in RSA and to understand the complex links between respiratory activity and arterial pressure, we determined the transfer functions between respiration, heart rate (HR), and phasic, systolic, diastolic, and pulse arterial pressures in 14 healthy subjects during 6-min periods in which the respiratory rate was controlled in a predetermined but erratic fashion. Pharmacological autonomic blockade with atropine, propranolol, and both, in combination with changes in posture, was used to characterize the sympathetic and vagal contributions to these relationships, as well as to dissect the direct mechanical links between respiration and arterial pressure from the effects of the RSA on arterial pressure. We found that 1) the pure sympathetic (standing + atropine) HR response is characterized by markedly reduced magnitude at frequencies > 0.1 Hz and a phase delay, whereas pure vagal (supine + propranolol) modulation of HR is characterized by higher magnitude at all frequencies and no phase delay; 2) both the mechanical links between respiration and arterial pressure and the RSA contribute significantly to the effects of respiration on arterial pressure; 3) the RSA contribution to arterial pressure fluctuations is significant for vagal but not for sympathetic modulation of HR; 4) the mechanical effects of respiration on arterial pressure are related to the negative rate of change of instantaneous lung volume; 5) the mechanical effects have a higher magnitude during systole than during diastole; and 6) the mechanical effects are larger in the standing than the supine position. Most of these findings can be explained by a simple model of circulatory control based on previously published experimental transfer functions from our laboratory.