Serizawa T, Mirsky I, Carabello B A, Grossman W
Am J Physiol. 1982 Apr;242(4):H633-7. doi: 10.1152/ajpheart.1982.242.4.H633.
The effects of gradually developing left ventricular pressure overload on diastolic myocardial stiffness were studied in a chronic moderate hypertrophy model. A snug aortic band was placed beneath the left coronary artery in six puppies 4.5 wk of age, and hemodynamic studies were performed 33.5 wk later. In all six dogs, moderate pressure gradients (10-58 mmHg) developed across the constriction, and angiographic area of the aortic constriction was significantly smaller than for a control group, 4.9 +/- 0.5 vs. 8.4 +/- 0.8 mm2/kg, (mean +/- SE, P less than 0.05). Increases occurred in left ventricular (LV) wall thickness (1.08 +/- 0.07 vs. 0.83 +/- 0.04 cm, P less than 0.05), LV wall mass (5.2 +/- 0.3 vs. 4.1 +/- 0.2 g/kg, P less than 0.05), and wall thickness-to-radius ratio (0.67 +/- 0.04 vs. 0.50 +/- 0.03, P less than 0.01), whereas no differences were noted in LV end-diastolic pressure (11 +/- 1 vs. 9 +/- 1 mmHg), LV end-diastolic volume (LVEDV, 2.06 +/- 0.22 vs. 2.35 +/- 0.15 ml/kg) or ejection fraction (71 +/- 4 vs. 71 +/- 3%). The values of LV wall mass, LVEDV, and aortic constriction are normalized to body weight. Diastolic LV myocardial stiffness was examined in terms of the elastic stiffness-stress relations. There were small and insignificant differences in end-diastolic stress (17.3 +/- 1.5 vs. 20.4 +/- 3.8 g/cm2), myocardial stiffness constant (Km, 13.7 +/- 5.6 vs. 11.2 +/- 3.3), and end-diastolic elastic stiffness (221 +/- 67 vs. 221 +/- 79 g/cm2) between hypertrophied and control hearts. No significant differences in the elastic stiffness of hypertrophied and normal muscle were observed over the common stress range of 5-25 g/cm2. We conclude that moderate left ventricular hypertrophy in chronic, gradually developing pressure overload is an adaptation process associated with normal myocardial stiffness.
在慢性中度肥大模型中,研究了逐渐发展的左心室压力超负荷对舒张期心肌僵硬度的影响。在6只4.5周龄的幼犬左冠状动脉下方放置一条紧贴的主动脉束带,33.5周后进行血流动力学研究。在所有6只犬中,缩窄处形成了中等压力梯度(10 - 58 mmHg),主动脉缩窄的血管造影面积显著小于对照组,分别为4.9±0.5 vs. 8.4±0.8 mm2/kg(均值±标准误,P<0.05)。左心室(LV)壁厚度增加(1.08±0.07 vs. 0.83±0.04 cm,P<0.05),LV壁质量增加(5.2±0.3 vs. 4.1±0.2 g/kg,P<0.05),壁厚度与半径之比增加(0.67±0.04 vs. 0.50±0.03,P<0.01),而LV舒张末期压力(11±1 vs. 9±1 mmHg)、LV舒张末期容积(LVEDV,2.06±0.22 vs. 2.35±0.15 ml/kg)或射血分数(71±4 vs. 71±3%)无差异。LV壁质量、LVEDV和主动脉缩窄的值均按体重进行了标准化。根据弹性僵硬度 - 应力关系检查了舒张期LV心肌僵硬度。肥厚心肌与对照心肌在舒张末期应力(17.3±1.5 vs. 20.4±3.8 g/cm2)、心肌僵硬度常数(Km,13.7±5.6 vs. 11.2±3.3)和舒张末期弹性僵硬度(221±67 vs. 221±79 g/cm2)方面存在微小且无统计学意义的差异。在5 - 25 g/cm2的共同应力范围内,未观察到肥厚心肌与正常心肌的弹性僵硬度有显著差异。我们得出结论,慢性、逐渐发展的压力超负荷导致的中度左心室肥大是一个与正常心肌僵硬度相关的适应过程。