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高血压大鼠的主动脉阻抗与顺应性

Aortic impedance and compliance in hypertensive rats.

作者信息

Zuckerman B D, Yin F C

机构信息

Department of Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205.

出版信息

Am J Physiol. 1989 Aug;257(2 Pt 2):H553-62. doi: 10.1152/ajpheart.1989.257.2.H553.

DOI:10.1152/ajpheart.1989.257.2.H553
PMID:2764136
Abstract

We compared aortic impedance and compliance in normotensive control and hypertensive Wistar rats. Hypertension was induced by unilateral nephrectomy plus steroid and salt water administration. After at least 8 wk of sustained hypertension (tail-cuff systolic pressures greater than 172 mmHg), open-chest ascending aortic micromanometric pressures and electromagnetic flows were measured. We used a frequency-modulated pacing method to enhance the energy content of the pressure and flow signals at specific low frequencies and their multiples. Impedance spectra were calculated using both Fourier series and spectral analysis methods. Compliance was calculated from the low-frequency impedance moduli, assuming a windkessel model for the arterial system. During pentobarbital sodium anesthesia under baseline conditions, the hypertensive rats had higher total resistance (219,000 vs. 126,000 dyn.s.cm-5), higher characteristic impedance (7,334 vs. 5,377 dyn.s.cm-5), larger first zero crossing of impedance phase angle (13.9 vs. 10 Hz), larger ratio of backward to forward pressure waves (0.67 vs. 0.48), and lower compliance (0.00498 vs. 0.00720 ml/mmHg) than controls. The differences between the groups were eliminated when the blood pressures of the hypertensive rats were normalized by vasodilation with nitroprusside or when the control rats were made hypertensive by vasoconstriction with phenylephrine. Thus the hemodynamic alterations appear to be secondary to the increased blood pressure. These base-line differences and the responses to vasoactive drugs are similar to findings in humans, suggesting that this rat model is a good hemodynamic model of human hypertension.

摘要

我们比较了正常血压对照Wistar大鼠和高血压Wistar大鼠的主动脉阻抗和顺应性。通过单侧肾切除加给予类固醇和盐水诱导高血压。在至少8周持续高血压(尾袖套收缩压大于172 mmHg)后,测量开胸状态下升主动脉微测压压力和电磁流量。我们使用调频起搏方法来增强特定低频及其倍数下压力和流量信号的能量含量。使用傅里叶级数和频谱分析方法计算阻抗谱。假设动脉系统为风箱模型,根据低频阻抗模量计算顺应性。在基线条件下戊巴比妥钠麻醉期间,高血压大鼠的总阻力较高(219,000 vs. 126,000 dyn.s.cm-5)、特征阻抗较高(7,334 vs. 5,377 dyn.s.cm-5)、阻抗相角的第一个零交叉点较大(13.9 vs. 10 Hz)、反向与正向压力波的比值较大(0.67 vs. 0.48),且顺应性较低(0.00498 vs. 0.00720 ml/mmHg)。当用硝普钠舒张使高血压大鼠血压正常化或用去氧肾上腺素收缩使对照大鼠血压升高时,两组之间的差异消除。因此,血流动力学改变似乎是血压升高的继发结果。这些基线差异以及对血管活性药物的反应与人类研究结果相似,表明该大鼠模型是人类高血压的良好血流动力学模型。

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