Hasenfuss G, Holubarsch C, Heiss H W, Meinertz T, Hofmann T, Just H
Department of Internal Medicine, University of Freiburg Medical School, F.R.G.
J Cardiovasc Pharmacol. 1989;14 Suppl 1:S69-74.
Enoximone may influence myocardial energetics by vasodilation, which may reduce and by inotropism which may increase myocardial energy demand. To separate both pharmacological properties, the influence of enoximone on myocardial oxygen consumption and its hemodynamic determinants was analyzed and compared to the effects of the pure vasodilator nitroprusside. The relationship between myocardial oxygen consumption and left ventricular hemodynamics was evaluated in 22 patients with idiopathic dilated cardiomyopathy (NYHA stages II-III). During control, myocardial oxygen consumption per beat [MVO2 (beat)] correlated closely with left ventricular systolic stress-time integral (STI) (r = 0.74; p less than 0.001). The ratio of MVO2 (beat) and STI was used as an inverse measure of the economy of myocardial contraction. Following nitroprusside (10 patients) the STI decreased by 35% (p less than 0.005) and MVO2 (beat) by 30% (p less than 0.005). MVO2 (beat)/STI did not significantly change. Following enoximone (12 patients), STI decreased by 60% (p less than 0.001), MVO2 (beat) by 19% (p less than 0.001), and MVO2 (beat)/STI increased from 1.31 +/- 0.16 to 2.72 +/- 0.78 nl.cm2/100 g.dyn.s (p less than 0.001). In summary, vasodilation by nitroprusside decreased MVO2 (beat) in proportion to its major determinant, STI; the economy of myocardial contraction remained unchanged. Compared to nitroprusside, enoximone reduced the economy of contraction. Thus, with enoximone, the energy-saving effect of vasodilation is counteracted by increased energy demand due to the inotropic stimulation of the myocardium. Global myocardial oxygen consumption depends on the balance of both pharmacological properties.
依诺昔酮可能通过血管舒张影响心肌能量代谢，这可能会降低心肌能量需求，同时也可能通过正性肌力作用增加心肌能量需求。为了区分这两种药理特性，分析了依诺昔酮对心肌氧耗及其血流动力学决定因素的影响，并与纯血管扩张剂硝普钠的作用进行了比较。在22例特发性扩张型心肌病（纽约心脏协会II - III级）患者中评估了心肌氧耗与左心室血流动力学之间的关系。在对照期间，每搏心肌氧耗[MVO2(搏)]与左心室收缩期应力 - 时间积分(STI)密切相关(r = 0.74；p < 0.001)。MVO2(搏)与STI的比值用作心肌收缩经济性的反向指标。给予硝普钠后(10例患者)，STI降低35%(p < 0.005)，MVO2(搏)降低30%(p < 0.005)。MVO2(搏)/STI无显著变化。给予依诺昔酮后(12例患者)，STI降低60%(p < 0.001)，MVO2(搏)降低19%(p < 0.001)，MVO2(搏)/STI从1.31±0.16增加至2.72±0.78 nl.cm2/100 g.dyn.s(p < 0.001)。总之，硝普钠引起的血管舒张按其主要决定因素STI的比例降低了MVO2(搏)；心肌收缩的经济性保持不变。与硝普钠相比，依诺昔酮降低了收缩的经济性。因此，对于依诺昔酮，血管舒张的节能作用被心肌正性肌力刺激导致的能量需求增加所抵消。整体心肌氧耗取决于这两种药理特性的平衡。
