Oxygen utilization during isovolumic pressure-volume loading: effects of prolonged extracorporeal circulation and cardioplegic arrest.
Oxygen utilization during isovolumic pressure-volume loading: effects of prolonged extracorporeal circulation and cardioplegic arrest.
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等容压力-容积负荷期间的氧气利用：延长体外循环和心脏停搏的影响。
DOI：
10.1016/s0003-4975(10)62697-5
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发表时间：
1986
期刊：
影响因子：
--
通讯作者：
Levitsky,S
中科院分区：
文献类型：
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作者：
Krukenkamp,I;Silverman,N;Sorlie,D;Pridjian,A;Feinberg,H;Levitsky,S
在体外循环支持的犬心脏中，等容峰值压力（PDP，mm Hg）和心肌耗氧量（MVO2，ml O2×10−2/次搏动/100 gm 左心室 [LV] 重量）在 2 小时钾心停跳（缺血，N = 7）或无缺血的常温灌注期间（对照，对照， N = 6）。将 MVO2 作为缺血性损伤标志物的敏感性与三磷酸腺苷 (ATP) 储存和收缩泵功能的保存进行比较。在舒张末期容积（5 至 35 ml）和舒张末期压力（0 至 18 mm Hg）的生理范围内，Frank-Starling 曲线在心脏停搏和长时间非缺血性灌注后均未下降。尽管 ATP 储存量分别减少了 26% 和 22%（分别为缺血组和对照组；不显着），但这些水平并不能区分心脏停跳和长时间灌注的影响。在两组干预前测量中，PDP 在 50 到 200 之间，与 MVO2 从 3.0 到 10.0 相关 (r= + 0.84)。心脏停跳后，在 75 至 200 mm Hg 的 PDP 范围内测量时，缺血后 MVO2 增加 137 ± 6% (p< 0.01)。在 PDP 低于 75、空跳心脏或接受非缺血性体外灌注的对照心脏中，这种变化并不明显。这些数据表明，与压力-体积关系的变化或腺嘌呤核苷酸储存的消耗相比，增加氧气利用以产生生理压力可能是缺血性损伤更敏感的指标。
In canine hearts supported by cardiopulmonary bypass, isovolumic peak developed pressure (PDP, mm Hg) and myocardial oxygen consumption (MVO2, ml O2× 10−2/beat/100 gm left ventricular [LV] weight) were determined at 5-ml increments of LV balloon inflation before and after either 2 hours of potassium cardioplegic arrest (ischemia, N = 7) or a comparable period of normothermic perfusion without ischemia (control, N = 6). The sensitivity of MVO2as a marker of ischemic injury was compared with preservation of both adenosine triphosphate (ATP) stores and systolic pump function. Over a physiological range of end-diastolic volumes (5 to 35 ml) and end-diastolic pressures (0 to 18 mm Hg), the Frank-Starling curves were not depressed following both cardioplegic arrest and prolonged nonischemic perfusion. Although ATP stores decreased by 26% and 22% (ischemia and control groups, respectively; not significant), these levels did not distinguish the effects of cardioplegic arrest from prolonged perfusion. At the preinterventional measurement in both groups, PDP between 50 and 200 correlated with MVO2from 3.0 to 10.0 (r= + 0.84). Following cardioplegic arrest, postischemic MVO2increased 137 ± 6% when measured over the PDP range of 75 to 200 mm Hg (p< 0.01). This change was not evident at a PDP of less than 75, in the empty beating heart, or in control hearts subjected to nonischemic extracorporeal perfusion. These data suggest that increased utilization of oxygen to develop physiological pressures may be a more sensitive indicator of ischemic injury than shifts in the pressure-volume relationship or depletion of adenine nucleotide stores.