Alterations in left ventricular mechanics, energetics, and contractile reserve in experimental heart failure.
Alterations in left ventricular mechanics, energetics, and contractile reserve in experimental heart failure.
复制标题
实验性心力衰竭中左心室力学、能量学和收缩储备的改变。
DOI：
10.1161/01.res.70.3.516
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发表时间：
1992
影响因子：
20.1
通讯作者：
Kass,DA
中科院分区：
文献类型：
--
作者：
Wolff,MR;deTombe,PP;Harasawa,Y;Burkhoff,D;Bier,S;Hunter,WC;Gerstenblith,G;Kass,DA
主要收缩和舒张特性的变化，收缩储备的限制，以及能量效率的改变与慢性起搏心动过速所见的左心室功能障碍的贡献进行了研究。7只犬（心力衰竭组）以每分钟250次的速度进行心室起搏，持续26.3 +/- 2.9天，并与单独的对照组（n = 8）进行比较。本研究采用离体的代谢支持心脏与计算机控制的负荷系统进行。测量压力-容积关系和心肌耗氧量（MVO 2），以评估心室收缩和舒张特性和效率（MVO 2与压力-容积面积[PVA]之间的关系）。与对照组相比，心力衰竭组的收缩功能降低，这是通过收缩末期压力-容积关系的斜率来评估的。（1.29 +/- 0.94 vs 2.71 +/- 0.98 mm Hg/ml，p <0.01），并在匹配应力下降低收缩末期硬度（956.1 +/- 123.5 vs 1，401.7 +/- 431.7 g/cm2，p <0.05）。心力衰竭患者的舒张室和心肌僵硬度没有改变，但无应激时的舒张期阻滞体积明显更大（33.3 +/- 3.9 vs 21.9 +/- 7.6 ml，p <0.01）。与对照心脏相比，心力衰竭患者对心率增加和外源性β-肾上腺素能刺激（盐酸多巴酚丁胺）的变力反应显著受损。最有趣的是，衰竭心脏的MVO 2-PVA关系斜率降低（2.1 +/- 1.1 vs 2.9 +/- 1.4 ml O2.mm Hg-1.ml-1.100 g left ventricular-1，p <0.001），表明化学机械能量转换效率增加。反映基础代谢和兴奋-收缩偶联的氧消耗的MVO 2-PVA关系的y截距在两组中没有变化，尽管心力衰竭心脏的收缩力降低。这些结果表明，在该心力衰竭模型中，心腔和心肌收缩力降低，扩张而不改变被动心肌特性，收缩储备受损，心脏效率发生新的变化。
The contributions of changes in primary systolic and diastolic properties, limitations of contractile reserve, and alterations in energy efficiency to the left ventricular dysfunction seen with chronic pacing tachycardia were investigated. Seven dogs (heart failure group) were ventricularly paced at 250 beats per minute for 26.3 +/- 2.9 days and compared with a separate control group (n = 8). STudies were performed with isolated, metabolically supported hearts coupled to a computer-controlled loading system. Pressure-volume relations and myocardial oxygen consumption (MVO2) were measured to assess chamber systolic and diastolic properties and efficiency (relation between MVO2 and pressure-volume area [PVA]). Systolic function was reduced in failure hearts versus controls as assessed by the slope of the end-systolic pressure-volume relation (1.29 +/- 0.94 versus 2.71 +/- 0.98 mm Hg/ml, p less than 0.01) and lowered end-systolic stiffness at a matched stress (956.1 +/- 123.5 versus 1,401.7 +/- 431.7 g/cm2, p less than 0.05). Diastolic chamber and myocardial stiffness were unaltered in failure hearts, but the unstressed diastolic-arrested volume was significantly larger (33.3 +/- 3.9 versus 21.9 +/- 7.6 ml, p less than 0.01). Inotropic response to increased heart rate and exogenous beta-adrenergic stimulation (dobutamine HCl) was significantly impaired in failure compared with control hearts. Most interestingly, failure hearts had a lowered slope of the MVO2-PVA relation (2.1 +/- 1.1 versus 2.9 +/- 1.4 ml O2.mm Hg-1.ml-1.100 g left ventricle-1, p less than 0.001), indicating increased efficiency of chemomechanical energy conversion. The y intercept of the MVO2-PVA relation, which reflects oxygen costs of basal metabolism and excitation-contraction coupling, was unchanged in the two groups despite decreased contractility of the heart failure hearts. These results demonstrate reduced chamber and myocardial contractility, dilatation without alteration of passive myocardial properties, impaired contractile reserve, and novel alterations in cardiac efficiency in this model of heart failure.