Hasenfuss G, Holubarsch C, Heiss H W, Meinertz T, Bonzel T, Wais U, Lehmann M, Just H
Department of Internal Medicine, University of Freiburg, Medical School, FRG.
Circulation. 1989 Jul;80(1):51-64. doi: 10.1161/01.cir.80.1.51.
Cardiotonic agents influence myocardial energy consumption by vasodilation, which may reduce energy demand, and by inotropism, which may increase it. To distinguish between the two effects, myocardial oxygen consumption must be analyzed in relation to its hemodynamic determinants. The coupling of myocardial oxygen consumption with its determinants was investigated in 22 patients with idiopathic dilated cardiomyopathy (NYHA Class II and III). Predicted myocardial oxygen consumption by the pressure-work index, the Bretschneider index, and the pressure-volume area correlated moderately with measured myocardial oxygen consumption (r = 0.57, p less than 0.001; r = 0.52, p less than 0.005; and r = 0.63, p less than 0.001). Multiple regression analysis, including left ventricular peak systolic wall stress, systolic stress-time integral, pressure-volume work, maximum rate of left ventricular pressure rise, and mean velocity of circumferential fiber shortening indicated that systolic stress-time integral is the major determinant of myocardial oxygen consumption (r = 0.75, p less than 0.001) in these patients. Enoximone, a phosphodiesterase inhibitor, has an inotropic and a vasodilating effect. To investigate the inotropic portion of the energy cost of this phosphodiesterase inhibitor, the influence of enoximone on myocardial oxygen consumption and systolic stress-time integral was compared with the effects of nitroprusside, which is a vasodilator only. Nitroprusside (10 patients) and enoximone (12 patients) reduced left ventricular systolic stress-time integral from 109 +/- 22 to 71 +/- 21 (p less than 0.005) and from 104 +/- 23 to 42 +/- 10 (p less than 0.001) 10(3) dynes.sec/cm2, respectively. Myocardial oxygen consumption decreased from 159 +/- 44 to 112 +/- 23 (p less than 0.005) and from 134 +/- 28 to 109 +/- 21 (p less than 0.001) microliters/beat/100 g, respectively. In both groups, there was a significant correlation between the decrease in myocardial oxygen consumption and the decrease in systolic stress-time integral. The slopes of the respective linear regression lines were significantly different (1.27 for nitroprusside and 0.51 nl.cm2/100 g.dynes.sec for enoximone, p less than 0.05), indicating a smaller decrease of myocardial oxygen consumption for a given decrease of stress-time integral with enoximone. Applying the pressure-work index or the pressure-volume area instead of systolic stress-time integral yielded comparable results. Thus, vasodilation reduces myocardial oxygen consumption in proportion to the reduction of stress-time integral. With enoximone, the energy-saving effect of vasodilation is counteracted in part by the increased energy d
强心剂通过血管舒张影响心肌能量消耗，这可能会降低能量需求，也通过变力作用影响心肌能量消耗，这可能会增加能量需求。为了区分这两种效应，必须结合血流动力学决定因素来分析心肌氧消耗。对22例特发性扩张型心肌病（纽约心脏协会II级和III级）患者的心肌氧消耗与其决定因素之间的耦合关系进行了研究。通过压力 - 功指数、布雷tschneider指数和压力 - 容积面积预测的心肌氧消耗与实测心肌氧消耗中度相关（r = 0.57，p < 0.001；r = 0.52，p < 0.005；r = 0.63，p < 0.001）。多元回归分析，包括左心室收缩期峰值壁应力、收缩期应力 - 时间积分、压力 - 容积功、左心室压力上升最大速率和圆周纤维缩短平均速度，表明收缩期应力 - 时间积分是这些患者心肌氧消耗的主要决定因素（r = 0.75，p < 0.001）。依诺昔酮是一种磷酸二酯酶抑制剂，具有正性肌力和血管舒张作用。为了研究这种磷酸二酯酶抑制剂能量消耗中的正性肌力部分，将依诺昔酮对心肌氧消耗和收缩期应力 - 时间积分的影响与仅作为血管扩张剂的硝普钠的作用进行了比较。硝普钠组（10例患者）和依诺昔酮组（12例患者）的左心室收缩期应力 - 时间积分分别从109±22降至71±21（p < 0.005）和从104±23降至42±10（p < 0.001）10³达因·秒/平方厘米。心肌氧消耗分别从159±44降至112±23（p < 0.005）和从134±28降至109±21（p < 0.001）微升/搏/100克。在两组中，心肌氧消耗的降低与收缩期应力 - 时间积分的降低之间均存在显著相关性。各自线性回归线的斜率显著不同（硝普钠为1.27，依诺昔酮为0.51纳升·平方厘米/100克·达因·秒，p < 0.05），表明在应力 - 时间积分给定降低的情况下，依诺昔酮导致的心肌氧消耗降低幅度较小。使用压力 - 功指数或压力 - 容积面积代替收缩期应力 - 时间积分也得到了类似结果。因此，血管舒张按应力 - 时间积分的降低比例降低心肌氧消耗。使用依诺昔酮时，血管舒张的节能作用部分被增加的能量消耗抵消。
