Mitchell G F, Pfeffer M A, Finn P V, Pfeffer J M
Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass 02115, USA.
Circulation. 1996 Dec 1;94(11):2923-9. doi: 10.1161/01.cir.94.11.2923.
Converting enzyme inhibitors are more effective than arteriolar vasodilators at regressing left ventricular hypertrophy in spontaneously hypertensive rats (SHR), possibly because of nonhemodynamic factors. However, the pulsatile component of hemodynamic load has not been evaluated in this model.
We measured pulsatile hemodynamics in 18-month-old male SHR after 6 months of therapy with either zofenopril (Z), hydralazine (H), or water (W). Hydralazine and zofenopril reduced mean arterial pressure comparably (W, 106 +/- 23 versus H, 81 +/- 12 versus Z, 84 +/- 18 mm Hg, P = .002) yet had a differential effect on the ratio of left ventricular weight to body weight (W, 3.9 +/- 0.5 versus H, 3.3 +/- 0.4 versus Z, 2.4 +/- 0.2 g/kg, P < .005). Hydralazine-treated SHR had increased characteristic impedance (P = .0011) and a persistently low ratio of the reflected-wave transit time to left ventricular ejection time (P < .001), which contributed to early and late systolic loading, respectively, of the left ventricle. Consequently, only zofenopril-treated SHR had a significant reduction in left ventricular systolic force-time integral (P = .02), a measure of total ventricular load. There were no differences in systolic stress-time integral, suggesting that mass was appropriate to load when all elements of steady-flow and pulsatile load were considered.
A blunted reduction in total left ventricular load, due to increased pulsatile load in SHR treated with hydralazine, provided a hemodynamic basis for the differential regression of hypertrophy in this model of genetic hypertension.
在自发性高血压大鼠（SHR）中，转换酶抑制剂在使左心室肥厚消退方面比小动脉血管扩张剂更有效，这可能是由于非血流动力学因素。然而，在该模型中尚未评估血流动力学负荷的脉动成分。
我们在18月龄雄性SHR接受佐芬普利（Z）、肼屈嗪（H）或水（W）治疗6个月后测量了脉动血流动力学。肼屈嗪和佐芬普利降低平均动脉压的程度相当（W组，106±23；H组，81±12；Z组，84±18 mmHg，P = 0.002），但对左心室重量与体重之比有不同影响（W组，3.9±0.5；H组，3.3±0.4；Z组，2.4±0.2 g/kg，P < 0.005）。接受肼屈嗪治疗的SHR特征阻抗增加（P = 0.0011），反射波传播时间与左心室射血时间的比值持续较低（P < 0.001），这分别导致左心室早期和晚期收缩期负荷增加。因此，只有接受佐芬普利治疗的SHR左心室收缩力 - 时间积分有显著降低（P = 0.02），这是心室总负荷的一个指标。收缩期应力 - 时间积分没有差异，表明在考虑稳定流和脉动负荷的所有因素时，心肌质量与负荷相适应。
在肼屈嗪治疗的SHR中，由于脉动负荷增加导致左心室总负荷降低不明显，为该遗传性高血压模型中肥厚的差异消退提供了血流动力学基础。
