Saul J P, Berger R D, Albrecht P, Stein S P, Chen M H, Cohen R J
Harvard-Massachusetts Institute of Technology, Division of Health Sciences and Technology, Cambridge 02139.
Am J Physiol. 1991 Oct;261(4 Pt 2):H1231-45. doi: 10.1152/ajpheart.1991.261.4.H1231.
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 greater than 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 teh 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.
我们之前已经证明，传递函数分析可用于精确表征正常人体的呼吸性窦性心律不齐（RSA）。为了进一步研究自主神经系统在RSA中的作用，并了解呼吸活动与动脉血压之间的复杂联系，我们测定了14名健康受试者在6分钟内呼吸、心率（HR）与相位、收缩压、舒张压及脉压之间的传递函数，在此期间呼吸频率以预定但不规则的方式进行控制。使用阿托品、普萘洛尔以及二者联合进行药理学自主神经阻滞，并结合体位变化，以表征交感神经和迷走神经对这些关系的贡献，同时区分呼吸与动脉血压之间的直接机械联系以及RSA对动脉血压的影响。我们发现：1）纯交感神经（站立+阿托品）的心率反应表现为频率大于0.1Hz时幅度显著降低且存在相位延迟，而纯迷走神经（仰卧+普萘洛尔）对心率的调节在所有频率下幅度更高且无相位延迟；2）呼吸与动脉血压之间的机械联系以及RSA均对呼吸对动脉血压的影响有显著贡献；3）RSA对动脉血压波动的贡献在迷走神经调节心率时显著，而在交感神经调节心率时不显著；4）呼吸对动脉血压的机械作用与瞬时肺容积的负变化率有关；5）收缩期的机械作用幅度高于舒张期；6）站立位时的机械作用大于仰卧位。基于我们实验室之前发表的实验传递函数，这些发现大多可用一个简单的循环控制模型来解释。
