Equipotent antihypertensive agents variously affect pulsatile hemodynamics and regression of cardiac hypertrophy in spontaneously hypertensive rats.
Equipotent antihypertensive agents variously affect pulsatile hemodynamics and regression of cardiac hypertrophy in spontaneously hypertensive rats.
复制标题
等效抗高血压药物对自发性高血压大鼠的脉动血流动力学和心脏肥大的消退有不同的影响。
DOI：
10.1161/01.cir.94.11.2923
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发表时间：
1996
期刊：
影响因子：
37.8
通讯作者：
Pfeffer,JM
中科院分区：
文献类型：
--
作者：
Mitchell,GF;Pfeffer,MA;Finn,PV;Pfeffer,JM
转换酶抑制剂在逆转自发性高血压大鼠（SHR）左心室肥厚方面比小动脉血管扩张剂更有效，这可能与非血流动力学因素有关。然而，血液动力学负荷的脉动分量尚未在此model.Methods和ResultsWe测量脉动血流动力学在18个月大的男性SHR 6个月后的治疗与佐芬普利（Z），肼苯哒嗪（H），或水（W）。肼苯哒嗪和佐芬普利降低平均动脉压100倍（W，106±23 vs H，81±12 vs Z，84±18 mm Hg，P= 0.002），但对左心室重量/体重比值的影响不同（W，3.9±0.5 vs H，3.3±0.4 vs Z，2.4±0.2 g/kg，P<0.005）。肼屈嗪治疗的SHR的特征阻抗增加（P= 0.0011），反射波传导时间与左心室射血时间的比值持续较低（P<0.001），这分别导致左心室收缩早期和晚期负荷。因此，只有佐芬普利治疗的SHR的左心室收缩力-时间积分显著降低（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，这表明质量是适当的负荷时，所有元素的稳定流和脉动负荷被认为considered.ConclusionsA钝减少左心室总负荷，由于增加脉动负荷在SHR治疗肼苯哒嗪，提供了一个血液动力学基础的差异回归的肥大在这个模型中的遗传性高血压。
BackgroundConverting 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.Methods and ResultsWe 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.ConclusionsA 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.