Wang M, Evans J, Knapp C
Center for Biomedical Engineering, University of Kentucky, Lexington 40506-0070, USA.
IEEE Trans Biomed Eng. 1995 Jul;42(7):708-17. doi: 10.1109/10.391170.
The role of heart rate in buffering and/or generating aortic pressure (AP) oscillations that occur at rest and in response to oscillatory blood volume shifts was studied. Six supine dogs with chronic AV blockade were used to examine: 1) resting HR and AP spectra when the ventricular rate was controlled by atrial depolarization (natural sinus rhythm); 2) resting AP and stroke volume (SV) spectra when the heart was AV sequentially paced at 60, 120, and 180 bpm before and after ganglionic blockade; and 3) the frequency response characteristics of AP and SV to whole-body sinusoidal acceleration (+/- 2gz, 0.008-0.23 Hz) at each heart rate before and after ganglionic blockade. During atrial regulation of HR, the spectra of both AP and HR had dominant peaks located at the breathing frequency (0.2-0.4 Hz) and relatively smaller peaks centered at approximately 0.05 Hz. During constant heart rate pacing, the spectra of AP had a dominant component at approximately 0.05 Hz. The power of this component was: 1) larger than during atrial regulation, 2) increased with increasing pacing rate, and 3) abolished by ganglionic blockade. There was no effect of pacing rate or ganglionic blockade on SV spectra. During oscillatory acceleration, AP regulation in the heart paced dogs was frequency dependent. Regions of good regulation occurred below 0.016 Hz and above 0.1 Hz, and poor regulation between 0.035 and 0.075 Hz centered at approximately 0.05 Hz. The oscillations in the poor regulation region were enhanced by increased pacing rate. After ganglionic blockade, the frequency response of AP was primarily hydraulic (low-pass). The frequency response of SV had a neural component. We conclude that: 1) resting AP fluctuations at respiratory frequencies resulted from respiration-linked HR variation; 2) the 0.05-Hz fluctuations in AP during rest and the poor regulation of AP at 0.05 Hz during acceleration resulted from a peripheral vascular response that lagged disturbances by approximately 10 s; 3) HR regulation was important in minimizing AP variation in the 0.05-Hz region both at rest and during oscillatory acceleration; and 4) inotropic control of SV was an important component of AP regulation during low-frequency acceleration.
研究了心率在缓冲和/或产生静息时以及响应振荡性血容量变化时出现的主动脉压力（AP）振荡中的作用。使用六只患有慢性房室传导阻滞的仰卧位犬来研究：1）当心室率由心房去极化控制（自然窦性心律）时的静息心率和AP频谱；2）在神经节阻断前后，心脏以60、120和180次/分钟的频率进行房室顺序起搏时的静息AP和每搏量（SV）频谱；3）在神经节阻断前后，每个心率下AP和SV对全身正弦加速度（±2gz，0.008 - 0.23 Hz）的频率响应特性。在心率的心房调节期间，AP和心率的频谱都有位于呼吸频率（0.2 - 0.4 Hz）的主导峰以及以约0.05 Hz为中心的相对较小的峰。在恒定心率起搏期间，AP频谱在约0.05 Hz处有一个主导成分。该成分的功率：1）比心房调节期间大；2）随着起搏频率增加而增加；3）被神经节阻断消除。起搏频率或神经节阻断对SV频谱没有影响。在振荡性加速期间，心脏起搏犬的AP调节是频率依赖性的。良好调节区域出现在0.016 Hz以下和0.1 Hz以上，而在约0.05 Hz为中心的0.035至0.075 Hz之间调节较差。调节较差区域的振荡通过增加起搏频率而增强。神经节阻断后，AP的频率响应主要是液压性的（低通）。SV的频率响应有一个神经成分。我们得出结论：1）呼吸频率下的静息AP波动是由与呼吸相关的心率变化引起的；2）静息时AP的0.05 Hz波动以及加速期间0.05 Hz时AP调节较差是由外周血管反应引起的，该反应使干扰滞后约10秒；3）心率调节对于在静息和振荡性加速期间最小化0.05 Hz区域的AP变化很重要；4）在低频加速期间，SV的变力性控制是AP调节的一个重要组成部分。
