Metabolic support as an adjunct to inotropic support in the hypoperfused heart.
Metabolic support as an adjunct to inotropic support in the hypoperfused heart.
复制标题
代谢支持作为低灌注心脏正性肌力支持的辅助手段。
DOI：
10.1006/jmcc.2000.1297
复制
发表时间：
2001
期刊：
影响因子：
--
通讯作者：
Apstein,CS
中科院分区：
文献类型：
--
作者：
Saupe,KW;Eberli,FR;Ingwall,JS;Apstein,CS
在严重低流量缺血的情况下，心肌的功输出低，对无氧糖酵解的依赖性高，增加心肌葡萄糖和胰岛素的供应是心脏保护。我们的目标是确定这种“代谢支持”策略是否在接受正性肌力刺激的中度低灌注心脏中也具有心脏保护作用，即当心肌工作接近正常，并且对无氧糖酵解的依赖性最小时。在20只离体大鼠心脏中，用含红细胞的灌注液（红细胞压积40%）灌注，除正常水平的乳酸和游离脂肪酸外，还加入正常（5 mM，15μ U/ml）或升高（19.5 mM，250 μ U/ml）的葡萄糖和胰岛素，测定了等容左室功能和心脏能量学（~（31）P-NMR波谱）。将冠状动脉血流降低至正常水平的30%，左心室压力降低50%。给予多巴酚丁胺40分钟可使发展压恢复至基线的95±13%，但使舒张压增加23±6 mmHg，[ATP]降低44± 6%。葡萄糖和胰岛素阻止了舒张末期压的增加，[ATP]仅下降了14± 3%。尽管心脏能量学和舒张功能有了这些改善，但在低灌注期间或之后增加葡萄糖和胰岛素并不能改善左心室压力。我们的结论是，强心剂支持的低灌注心脏可以引起新的舒张功能障碍，但这种舒张功能障碍可以消除保留心肌高能量磷酸盐增加葡萄糖和胰岛素。
In situations such as severe low-flow ischemia, where myocardial work output is low and dependence on anaerobic glycolysis is high, increasing the myocardial supply of glucose and insulin is cardioprotective. Our goal was to determine whether this strategy of “metabolic support” would also be cardioprotective in the moderately hypoperfused heart receiving inotropic stimulation, i.e. when myocardial work was near normal, and reliance on anaerobic glycolysis was minimal. Isovolumic left ventricular performance and cardiac energetics (31P-NMR spectroscopy) were measured in 20 isolated rat hearts perfused with red blood cell containing perfusate (hematocrit 40%) with either normal (5 m M , 15μ U/ml) or increased (19.5 m M , 250 μ U/ml) glucose and insulin in addition to normal levels of lactate and free fatty acids. Lowering global coronary flow to 30% of normal decreased left ventricle developed pressure by 50%. Administering dobutamine for 40 min restored developed pressure to 95±13% of baseline but caused diastolic pressure to increase by 23±6 mmHg and [ATP] to decrease by 44±6%. Glucose and insulin prevented the increase in end-diastolic pressure, and [ATP] fell by only 14±3%. Despite these improvements in cardiac energetics and diastolic function, left ventricle developed pressure was not improved by increased glucose and insulin during, or after the hypoperfusion. We conclude that inotropic support of the hypoperfused heart can cause new diastolic dysfunction, but that this diastolic dysfunction can be eliminated by preserving myocardial high-energy phosphates with increased glucose and insulin.