Shibata Shigeki, Zhang Rong, Hastings Jeff, Fu Qi, Okazaki Kazunobu, Iwasaki Ken-Ichi, Levine Benjamin D
Institute for Exercise and Environmental Medicine, 7232 Greenville Ave, Suite 435, Dallas, TX 75231, USA.
Am J Physiol Heart Circ Physiol. 2006 Nov;291(5):H2142-51. doi: 10.1152/ajpheart.00157.2006. Epub 2006 Jun 9.
Cardiovascular variability reflects autonomic regulation of blood pressure (BP) and heart rate (HR). However, systolic BP (SBP) variability also may be induced by fluctuations in stroke volume through left ventricular end-diastolic pressure (LVEDP) variability via dynamic ventricular-arterial coupling during respiration. We hypothesized that dynamic ventricular-arterial coupling is modulated by changes in left ventricular compliance associated with altered preload and that a cascade control mechanism of ventricular-arterial coupling with arterial-cardiac baroreflex function contributes to the genesis of cardiovascular variability at the respiratory frequency. Seven healthy young subjects underwent 6-min recordings of beat-by-beat LVEDP, SBP, and HR in the supine position with controlled respiration at 0.2 Hz during hyper- and hypovolemia. Spectral and transfer function analysis of these variables was conducted between 0.18 and 0.22 Hz. Dynamic ventricular-arterial coupling gain (Gain LVEDP-SBP) was smaller by 25% (P = 0.009) during hypervolemia than during hypovolemia, whereas arterial-cardiac baroreflex function gain (Gain SBP-HR) was similar. As predicted from a cascade model, a linear relationship between Gain LVEDP-HR and LVEDP-SBP times Gain SBP-HR was identified (R(2) = 0.93, P < 0.001). Gain LVEDP-HR was smaller by 40% (P = 0.04) during hypervolemia than during hypovolemia, leading to a reduction in spectral power of HR variability by 45% (P = 0.08). We conclude that dynamic ventricular-arterial coupling gain is reduced during hypervolemia because of a decrease in left ventricular compliance. A cascade model of ventricular-arterial coupling with the arterial-cardiac baroreflex contributes to the genesis of cardiovascular variability at the respiratory frequency.
心血管变异性反映了自主神经系统对血压（BP）和心率（HR）的调节。然而，收缩压（SBP）变异性也可能由呼吸过程中通过左心室舒张末期压力（LVEDP）变异性引起的每搏输出量波动，经动态心室 - 动脉耦合作用而诱发。我们假设动态心室 - 动脉耦合受与前负荷改变相关的左心室顺应性变化的调节，并且心室 - 动脉耦合与动脉 - 心脏压力反射功能的级联控制机制有助于呼吸频率下心血管变异性的产生。七名健康年轻受试者在高血容量和低血容量状态下，于仰卧位以0.2 Hz的频率进行受控呼吸，记录6分钟逐搏的LVEDP、SBP和HR。对这些变量在0.18至0.22 Hz之间进行频谱和传递函数分析。高血容量时动态心室 - 动脉耦合增益（增益LVEDP - SBP）比低血容量时小25%（P = 0.009），而动脉 - 心脏压力反射功能增益（增益SBP - HR）相似。正如从级联模型预测的那样，确定了增益LVEDP - HR与LVEDP - SBP乘以增益SBP - HR之间的线性关系（R(2) = 0.93，P < 0.001）。高血容量时增益LVEDP - HR比低血容量时小40%（P = 0.04），导致心率变异性的频谱功率降低45%（P = 0.08）。我们得出结论，高血容量时由于左心室顺应性降低，动态心室 - 动脉耦合增益减小。心室 - 动脉耦合与动脉 - 心脏压力反射的级联模型有助于呼吸频率下心血管变异性的产生。
