Yasumura Y, Nozawa T, Futaki S, Tanaka N, Suga H
Department of Cardiovascular Dynamics, National Cardiovascular Center Research Institute, Osaka, Japan.
Am J Physiol. 1989 May;256(5 Pt 2):H1289-94. doi: 10.1152/ajpheart.1989.256.5.H1289.
We studied whether end-diastolic volume (EDV) would affect myocardial oxygen consumption (VO2) of mechanically unloaded contraction in the cross-circulated dog heart, as expected from the concept of the myocardial length-dependent activation. We made preloaded but maximally unloaded contractions from different EDVs by quickly releasing ventricular volume to eliminate systolic pressure development and hence to minimize the VO2 for mechanical load during the contraction. We then studied the relation between VO2 and EDV. The VO2 of the almost unloaded contraction from a relatively large EDV slightly exceeded the VO2 of the isovolumic contraction at V0, where V0 is the volume at which peak isovolumic pressure was zero. However, the excess VO2 could be ascribed to the residual systolic pressure-volume area (PVA) adversely produced from the large EDV, where PVA is a measure of the total mechanical energy generated during contraction. Therefore, we considered that VO2 was practically little dependent on EDV. We interpreted this finding as an indication that an increase, if any, in VO2 due to the length-dependent activation of the excitation-contraction coupling was practically negligible in the whole heart preparation.
我们研究了舒张末期容积(EDV)是否会影响交叉循环犬心脏中机械卸载收缩的心肌耗氧量(VO2),这是根据心肌长度依赖性激活的概念所预期的。我们通过快速释放心室容积来消除收缩压的产生,从而在收缩过程中最大程度地减少机械负荷的VO2,从不同的EDV进行预负荷但最大程度卸载的收缩。然后我们研究了VO2与EDV之间的关系。来自相对较大EDV的几乎卸载收缩的VO2略超过V0时等容收缩的VO2,其中V0是等容压力峰值为零时的容积。然而,过量的VO2可归因于由大EDV不利产生的残余收缩压-容积面积(PVA),其中PVA是收缩过程中产生的总机械能的一种度量。因此,我们认为VO2实际上几乎不依赖于EDV。我们将这一发现解释为一个迹象,即由于兴奋-收缩偶联的长度依赖性激活导致的VO2增加(如果有的话)在整个心脏制备中实际上可以忽略不计。