Chang K C, Hsieh K S, Kuo T S, Chen H I
Department and Institute of Electrical Engineering, National Taiwan University, Taipei, Republic of China.
Cardiovasc Res. 1990 Sep;24(9):719-26. doi: 10.1093/cvr/24.9.719.
The aim of the study was (1) to determine the difference in aortic input impedance and derived parameters between hypertensives and normotensives; and (2) to assess the acute effects of nifedipine on the aortic impedance, compliance, and resistance in patients with hypertension.
A high fidelity multisensor catheter (Millar) was used to obtain the aortic pressure and flow signals for impedance analysis. The acute effects of nifedipine on the impedance parameters were evaluated at steady state before and after (10-30 min) a sublingual dose of 10 mg.
The patients included seven normotensive (mean blood pressure, 97 mm Hg) and nine hypertensive (mean blood pressure, 135 mm Hg), age matched, ethnic Chinese. Patients with clinical evidence of heart failure and valvular or congenital heart diseases were excluded.
Pulsatile aortic flow and pressure were measured by Millar catheter inserted into the ascending aorta. Cross sectional area of aorta was estimated by echocardiograms. Cardiac output was determined by Fick principle with an oximeter. These data were subjected to Fourier analysis for impedance spectra. In comparison with normotensives, hypertensives had increased peripheral vascular resistance R, at 2751(705) v 1651(363) dyne.s.cm-5; increased characteristic impedance Zc, at 193(64) v 122(27) dyne.s.cm-5; and increased first zero crossing frequency of impedance phase angle fo, at 4.8(0.9) v 3.4(0.7) Hz. Arterial compliances corresponding to peak systolic pressure Cs were lower, at 0.32(0.19) v 0.90(0.32) ml.mm Hg-1, as was mean pressure Cm, at 0.55(0.25) v 1.24(0.38) ml.mm Hg-1, and end diastolic pressure Cd, at 0.83(0.29) v 1.65(0.44) ml.mm Hg-1. Although the values of external ventricular hydraulic power were higher in hypertensive subjects, the difference was not statistically significant. Nifedipine administration in 7/9 hypertensives significantly reduced R, from 2806(721) to 2433(664) dyne.s.cm-5; mean aortic pressure Pm, from 138(22) to 112(12) mm Hg; total external ventricular power Wt, from 1452(306) to 1121(135) mW; and steady external power Ws, from 1251(310) to 939(119) mW; but did not reduce Zc, fo, Cs, Cm, Cd, and oscillatory external power Wo.
The results indicate that (1) the stiffness of proximal aorta and vascular tone of peripheral arterioles are higher in hypertensives than in normotensives; (2) in hypertensive subjects, sublingual administration of nifedipine reduces the arterial pressure and peripheral arteriolar tone, but not the stiffness of proximal aorta; (3) the decrease in total external ventricular power in hypertensives treated with nifedipine results from a reduction in the steady, but not the oscillatory, component of hydraulic external ventricular power.
本研究的目的是（1）确定高血压患者与血压正常者之间主动脉输入阻抗及衍生参数的差异；（2）评估硝苯地平对高血压患者主动脉阻抗、顺应性和阻力的急性影响。
使用高保真多传感器导管（Millar）获取主动脉压力和血流信号以进行阻抗分析。在舌下含服10 mg硝苯地平之前和之后（10 - 30分钟）的稳态下评估硝苯地平对阻抗参数的急性影响。
患者包括7名血压正常者（平均血压97 mmHg）和9名高血压患者（平均血压135 mmHg），年龄匹配，均为华裔。排除有心力衰竭以及瓣膜或先天性心脏病临床证据的患者。
通过插入升主动脉的Millar导管测量搏动性主动脉血流和压力。通过超声心动图估计主动脉横截面积。采用血氧计根据Fick原理测定心输出量。对这些数据进行傅里叶分析以获得阻抗谱。与血压正常者相比，高血压患者的外周血管阻力R增加，分别为2751（705）与1651（363）达因·秒·厘米⁻⁵；特征阻抗Zc增加，分别为193（64）与122（27）达因·秒·厘米⁻⁵；阻抗相角的第一个过零频率fo增加，分别为4.8（0.9）与3.4（0.7）Hz。对应于收缩压峰值Cs的动脉顺应性较低，分别为0.32（0.19）与0.90（0.32）ml·mmHg⁻¹，平均压力Cm也较低，分别为0.55（0.25）与1.24（0.38）ml·mmHg⁻¹，舒张末期压力Cd同样较低，分别为0.83（0.29）与1.65（0.44）ml·mmHg⁻¹。尽管高血压受试者的心室外部水力功率值较高，但差异无统计学意义。9名高血压患者中有7名服用硝苯地平后，R从2806（721）显著降至2433（664）达因·秒·厘米⁻⁵；平均主动脉压力Pm从138（22）降至112（12）mmHg；总心室外部功率Wt从1452（306）降至1121（135）mW；稳态外部功率Ws从1251（310）降至939（119）mW；但未降低Zc、fo、Cs、Cm、Cd和振荡外部功率Wo。
结果表明，（1）高血压患者近端主动脉的僵硬度和外周小动脉的血管张力高于血压正常者；（2）在高血压受试者中，舌下含服硝苯地平可降低动脉压和外周小动脉张力，但不会降低近端主动脉的僵硬度；（3）硝苯地平治疗的高血压患者总心室外部功率的降低是由于心室外部水力功率稳态成分的降低，而非振荡成分的降低。
