Yaku H, Goto Y, Ohgoshi Y, Kawaguchi O, Oga K, Oka T, Suga H
Second Department of Surgery, Kyoto Prefectural University of Medicine, Japan.
J Thorac Cardiovasc Surg. 1993 Apr;105(4):679-88.
The purpose of the present study was to elucidate the mechanism of the difference in myocardial oxygen consumption between heating and fibrillating states during normothermia and hypothermia. In five isolated cross-circulated dog hearts, we measured left ventricular pressure at several ventricular volumes and myocardial oxygen consumption at V0 and V100, at which peak isovolumic pressures were zero and approximately 100 mm Hg, respectively, in beating and fibrillating states during normothermia and hypothermia (29 degrees C). As a measure of the total mechanical energy at V100, we obtained pressure-volume area in the beating state and equivalent pressure-volume area for fibrillation. We calculated equivalent heart rate as an estimate of the contraction frequency of individual myocytes in a fibrillating ventricle from myocardial oxygen consumption at V0 in the beating and fibrillating states. During normothermia, myocardial oxygen consumption per minute at V0 and V100 and myocardial oxygen consumption for mechanical purposes at V100 (myocardial oxygen consumption at V100-myocardial oxygen consumption at V0) were significantly higher during fibrillation than in the beating state. Equivalent pressure-volume area during fibrillation and pressure-volume area in the beating state at V100 were comparable, whereas equivalent heart rate during fibrillation was significantly higher than heart rate in the beating state. During hypothermia, myocardial oxygen consumption was comparable between beating and fibrillating states at V0, although myocardial oxygen consumption at V100 was slightly lower during fibrillation than in the beating state. Myocardial oxygen consumption for mechanical purposes during fibrillation was half of that in the beating state. Equivalent pressure-volume area was significantly smaller than pressure-volume area, whereas equivalent heart rate and heart rate were comparable. We conclude that during normothermia, higher myocardial oxygen consumption during fibrillation than in the beating state at V0 and V100 is attributable to the higher contraction frequency. During hypothermia the comparable myocardial oxygen consumption values at V0 are attributable to the comparable contraction frequencies, whereas slightly lower myocardial oxygen consumption during fibrillation at V100 is ascribed to the lower total mechanical energy.
本研究的目的是阐明正常体温和低温状态下加热和颤动状态中心肌耗氧量差异的机制。在五个离体交叉循环犬心脏中,我们测量了在正常体温和低温(29℃)下,跳动和颤动状态下几个心室容积时的左心室压力,以及V0和V100时的心肌耗氧量,其中V0和V100时等容压力峰值分别为零和约100mmHg。作为V100时总机械能的量度,我们获得了跳动状态下的压力-容积面积和颤动时的等效压力-容积面积。我们根据跳动和颤动状态下V0时的心肌耗氧量,计算等效心率,以估计颤动心室中单个心肌细胞的收缩频率。在正常体温下,V0和V100时每分钟的心肌耗氧量以及V100时用于机械目的的心肌耗氧量(V100时的心肌耗氧量-V0时的心肌耗氧量)在颤动时显著高于跳动状态。颤动时的等效压力-容积面积和V100时跳动状态下的压力-容积面积相当,而颤动时的等效心率显著高于跳动状态下的心率。在低温下,V0时跳动和颤动状态下的心肌耗氧量相当,尽管颤动时V100时的心肌耗氧量略低于跳动状态。颤动时用于机械目的的心肌耗氧量是跳动状态下的一半。等效压力-容积面积显著小于压力-容积面积,而等效心率和心率相当。我们得出结论,在正常体温下,V0和V100时颤动时心肌耗氧量高于跳动状态是由于收缩频率较高。在低温下,V0时相当的心肌耗氧量值归因于相当的收缩频率,而颤动时V100时略低的心肌耗氧量归因于较低的总机械能。