Tian R, Gaudron P, Neubauer S, Hu K, Ertl G
Medizinische Universitätsklinik Würzburg, Germany.
J Mol Cell Cardiol. 1996 Feb;28(2):321-30. doi: 10.1006/jmcc.1996.0030.
Progressive dilatation of left ventricle has been demonstrated in hearts post-infarction. However, the relationship of performance and energy consumption in chronically infarcted heart has not been clarified. To address this problem, we measured left ventricular pressure and oxygen consumption (MVO2) during stepwise increases in left ventricular filling volume in isolated isovolumic buffer-perfused rat hearts 8 weeks after let coronary artery ligation or sham-operation. Systolic pressure-volume area (PVA) was calculated as an estimate of total mechanical energy consumed by the heart. The MVO2-PVA relation was analysed to define the economy of the contractile machinery in surviving myocardium. Structural dilatation and reduced pressure generation in infarcted hearts were indicated by a rightward shift of pressure-volume curves and a reduced maximal developed pressure of the left ventricle (80 +/- 5 v 119 +/- 4 mmHg, P < 0.01) which was obtained at substantially higher left ventricular volume compared to control hearts (0.79 +/- 0.02 v 0.39 +/- 0.01 ml, P < 0.01). The slope of the MVO2-PVA relation was significantly lower in the infarcted compared to the control groups (1.02 +/- 0.16 v 1.44 +/- 0.10 10(-5) mlO2/mmHg/ml, P < 0.05), reflecting an increased efficiency of chemomechanical energy transduction in surviving myocardium. However, at the similar MVO2 ventricular pressure development was significantly lower in infarcted hearts due to the unfavorable geometry resulting from ventricular dilatation.
心肌梗死后的心脏已证实存在左心室的进行性扩张。然而，慢性梗死心脏的功能与能量消耗之间的关系尚未阐明。为解决这一问题，我们在左冠状动脉结扎或假手术8周后的离体等容缓冲液灌注大鼠心脏中，在逐步增加左心室充盈量的过程中测量了左心室压力和氧耗量（MVO2）。计算收缩压-容积面积（PVA）作为心脏消耗的总机械能的估计值。分析MVO2-PVA关系以确定存活心肌中收缩机制的经济性。梗死心脏中压力-容积曲线右移以及左心室最大发展压力降低（80±5对119±4 mmHg，P<0.01）表明结构扩张和压力产生减少，与对照心脏相比，这是在显著更高的左心室容积下获得的（0.79±0.02对0.39±0.01 ml，P<0.01）。与对照组相比，梗死组中MVO2-PVA关系的斜率显著更低（1.02±0.16对1.44±0.10 10(-5) mlO2/mmHg/ml，P<0.05），反映了存活心肌中化学机械能转换效率的提高。然而，在相似的MVO2时，由于心室扩张导致的不利几何形状，梗死心脏中的心室压力发展显著更低。
