Chiu W C, Kedem J, Scholz P M, Weiss H R
Department of Surgery, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, Piscataway.
Basic Res Cardiol. 1994 Mar-Apr;89(2):149-62. doi: 10.1007/BF00788734.
Despite apparently depressed function, stunned myocardium maintains oxygen consumption and has the capacity to increase contractility with inotropic stimulation. We hypothesized that during stunning, O2 demand is maintained because regional segment work is performed, but is asynchronous with global left ventricular contraction, and that inotropic stimulation would restore regional work and synchrony. Thirteen open-chest anesthetized dogs were subjected to three left anterior descending (LAD) coronary artery occlusions (10 min) and reperfusions (15 min) to produce regional myocardial stunning. Segment shortening and force development were measured independently and simultaneously in the LAD (experimental) region and circumflex (control) regions. Regional myocardial work was calculated as the integrated product of instantaneous force and shortening, during two periods: 1) over the entire cardiac cycle (Positive Work), and 2) limited to the systolic portion of the cardiac cycle (Systolic Work). Regional myocardial O2 consumption (MVO2) was calculated from regional blood flow (radiolabeled microspheres) and O2 saturation data (microspectrophotometry). Occlusion of the LAD produced a delay in onset of segment shortening in the ischemic region, but not in regional force development. A time delay of 67-81 ms persisted through the three stages of occlusions and reperfusions. Systolic regional work was depressed to a greater extent (924 +/- 182 to 149 +/- 118 gmmmin-1) than total positive regional work (1437 +/- 337 to 857 +/- 174 gmmmin-1). Regional subepicardial MVO2 in the stunned region was not different than in the control region (7.3 +/- 1.5 vs. 6.9 +/- 1.4 ml O2min-1100 g-1). Local infusion of isoproterenol reversed the delay in regional shortening from 73 +/- 7 to 21 +/- 8 ms, thereby augmenting systolic work (298%) more than positive work (60%), without a significant increase in MVO2 (7.3 +/- 1.5 to 10.5 +/- 3.2 ml O2min-1100 g-1). It is concluded that myocardial stunning decreases regional systolic work due to regional mechanical asynchrony, while MVO2 is used supported total positive work which was not significantly reduced. Isoproterenol restores regional work by restoring synchrony, without greatly affecting regional MVO2.
尽管功能明显降低,但顿抑心肌仍保持氧消耗,并且能够通过变力刺激增加收缩力。我们假设,在顿抑期间,由于进行了局部节段作功,氧需求得以维持,但与左心室整体收缩不同步,并且变力刺激将恢复局部作功和同步性。对13只开胸麻醉犬进行三次左前降支(LAD)冠状动脉闭塞(10分钟)和再灌注(15分钟),以产生局部心肌顿抑。在LAD(实验)区域和回旋支(对照)区域独立且同时测量节段缩短和力的产生。局部心肌作功计算为两个时期内瞬时力和缩短的积分乘积:1)在整个心动周期(正功),以及2)限于心动周期的收缩期部分(收缩期功)。局部心肌氧消耗(MVO2)根据局部血流(放射性标记微球)和氧饱和度数据(显微分光光度法)计算。LAD闭塞导致缺血区域节段缩短起始延迟,但局部力的产生无延迟。在闭塞和再灌注的三个阶段持续存在67 - 81毫秒的时间延迟。收缩期局部作功比总的局部正功降低程度更大(从924±182降至149±118克·毫米·分钟-1)(从1437±337降至857±174克·毫米·分钟-1)。顿抑区域的心外膜下局部MVO2与对照区域无差异(7.3±1.5对6.9±1.4毫升氧·分钟-1·100克-1)。局部输注异丙肾上腺素将局部缩短延迟从73±7毫秒逆转至21±8毫秒,从而使收缩期功增加(298%)超过正功增加(60%),而MVO2无显著增加(从7.3±1.5升至10.5±3.2毫升氧·分钟-1·100克-1)。结论是,心肌顿抑由于局部机械不同步而降低局部收缩期作功,而MVO2用于支持未显著降低的总的局部正功。异丙肾上腺素通过恢复同步性来恢复局部作功,而对局部MVO2影响不大。