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首页> 外文期刊>Cell Research >Reduced cardiac output is associated with decreased mitochondrial efficiency in the non-ischemic ventricular wall of the acute myocardial-infarcted dog.
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Reduced cardiac output is associated with decreased mitochondrial efficiency in the non-ischemic ventricular wall of the acute myocardial-infarcted dog.

机译：在急性心肌梗死犬的非缺血性心室壁中，心输出量的减少与线粒体效率的降低有关。

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Cardiogenic shock is the leading cause of death among patients hospitalized with acute myocardial infarction (MI). Understanding the mechanisms for acute pump failure is therefore important. The aim of this study is to examine in an acute MI dog model whether mitochondrial bio-energetic function within non-ischemic wall regions are associated with pump failure. Anterior MI was produced in dogs via ligation of left anterior descending (LAD) coronary artery, that resulted in an infract size of about 30% of the left ventricular wall. Measurements of hemodynamic status, mitochondrial function, free radical production and mitochondrial uncoupling protein 3 (UCP3) expression were determined over 24 h period. Hemodynamic measurements revealed a > 50% reduction in cardiac output at 24 h post infarction when compared to baseline. Biopsy samples were obtained from the posterior non-ischemic wall during acute infarction. ADP/O ratios for isolated mitochondria from non-ischemic myocardium at 6 h and 24 h were decreased when compared to the ADP/O ratios within the same samples with and without palmitic acid (PA). GTP inhibition of (PA)-stimulated state 4 respiration in isolated mitochondria from the non-ischemic wall increased by 7% and 33% at 6 h and 24 h post-infarction respectively when compared to sham and pre-infarction samples. This would suggest that the mitochondria are uncoupled and this is supported by an associated increase in UCP3 expression observed on western blots from these same biopsy samples. Blood samples from the coronary sinus measured by electron paramagnetic resonance (EPR) methods showed an increase in reactive oxygen species (ROS) over baseline at 6 h and 24 h post-infarction. In conclusion, mitochondrial bio-energetic ADP/O ratios as a result of acute infarction are abnormal within the non-ischemic wall. Mitochondria appear to be energetically uncoupled and this is associated with declining pump function. Free radical production may be associated with the induction of uncoupling proteins in the mitochondria.Cell Research (2006) 16: 297-305. doi:10.1038/sj.cr.7310037; published online 16 March 2006.
机译：心源性休克是住院急性心肌梗塞（MI）患者的主要死亡原因。因此，了解急性泵故障的机制很重要。这项研究的目的是在急性MI狗模型中检查非缺血性壁区域内的线粒体生物能功能是否与泵衰竭相关。结扎左前降支（LAD）冠状动脉可在犬中产生前壁MI，其梗阻面积约为左心室壁的30％。在24小时内测定血液动力学状态，线粒体功能，自由基产生和线粒体解偶联蛋白3（UCP3）表达。血流动力学测量显示，与基线相比，梗死后24 h心输出量减少> 50％。急性梗死时从非缺血性后壁获得活检样本。与具有和不具有棕榈酸（PA）的相同样品中的ADP / O相比，在6 h和24 h从非缺血性心肌分离的线粒体的ADP / O降低了。与假手术和梗死前样品相比，在梗死后6 h和24 h，来自非缺血性壁的孤立线粒体中（PA）刺激的状态4呼吸的GTP抑制分别增加了7％和33％。这表明线粒体是解偶联的，这由这些相同的活检样品的蛋白质印迹中观察到的UCP3表达的相关增加所支持。通过电子顺磁共振（EPR）方法测量的冠状窦血样显示，梗死后6 h和24 h的活性氧（ROS）超过基线。总之，急性缺血导致的线粒体生物能ADP / O比值在非缺血壁内异常。线粒体似乎没有能量耦合，这与泵功能下降有关。自由基的产生可能与线粒体中解偶联蛋白的诱导有关。CellResearch（2006）16：297-305。 doi：10.1038 / sj.cr.7310037;在线发布于2006年3月16日。

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