Vanoverschelde J L, Wijns W, Essamri B, Bol A, Robert A, Labar D, Cogneau M, Michel C, Melin J A
Division of Cardiology, University of Louvain Medical School, Brussels, Belgium.
Am J Physiol. 1993 Dec;265(6 Pt 2):H1884-92. doi: 10.1152/ajpheart.1993.265.6.H1884.
The relationship of myocardial O2 consumption (MVO2) to its potential hemodynamic and mechanical determinants was investigated in eight healthy normal volunteers at rest and during infusion of dobutamine (5-10 micrograms.kg-1.min-1). MVO2 was calculated from the monoexponential myocardial clearance of [1-11C]acetate with positron emission tomography, and left ventricular mechanical function was assessed by two-dimensional echocardiography. Infusion of dobutamine increased heart rate by 53%, the tension-time index by 31%, and the rate-pressure product by 116%. Cardiac output (+70%), left ventricular ejection fraction (+24%), total mechanical energy [systolic pressure-volume area, (PVA) +84%], and left ventricular pressure-work index (+100%) also increased during infusion of dobutamine. During infusion of dobutamine, MVO2 increased from 96 +/- 17 to 233 +/- 19 J.min-1.100 g left ventricle-1, while myocardial efficiency (the ratio of PVA to MVO2) decreased from 46 +/- 8 to 35 +/- 4% (P < 0.001 each). MVO2 was best correlated (P < 0.001) with the PVA (r = 0.92) and the pressure-work index (r = 0.92). Infusion of dobutamine also resulted in a significant parallel upward shift of the PVA-MVO2 relationship, indicative of an increase in PVA-independent MVO2. Our data indicate that, in human subjects, MVO2 is mainly related to systolic PVA and that inotropic stimulation with dobutamine results in decreased efficiency of contraction, such as that previously described in isolated hearts.
在8名健康正常志愿者静息状态下以及静脉输注多巴酚丁胺（5 - 10微克·千克⁻¹·分钟⁻¹）期间，研究了心肌氧耗（MVO2）与其潜在的血流动力学和机械决定因素之间的关系。通过正电子发射断层扫描利用[1 - ¹¹C]乙酸盐的单指数心肌清除率计算MVO2，并通过二维超声心动图评估左心室机械功能。输注多巴酚丁胺使心率增加53%，张力 - 时间指数增加31%，速率 - 压力乘积增加116%。多巴酚丁胺输注期间，心输出量（增加70%）、左心室射血分数（增加24%）、总机械能[收缩压 - 容积面积，(PVA)增加84%]以及左心室压力 - 功指数（增加100%）也增加。在多巴酚丁胺输注期间，MVO2从96±17增加至233±19焦·分钟⁻¹·100克左心室⁻¹，而心肌效率（PVA与MVO2的比值）从46±8降至35±4%（每项P < 0.001）。MVO2与PVA（r = 0.92）和压力 - 功指数（r = 0.92）相关性最佳（P < 0.001）。输注多巴酚丁胺还导致PVA - MVO2关系显著平行向上移位，表明与PVA无关的MVO2增加。我们的数据表明，在人体中，MVO2主要与收缩期PVA相关，并且多巴酚丁胺的正性肌力刺激导致收缩效率降低，如先前在离体心脏中所描述的那样。
