DISSOCIATION BETWEEN CONTRACTILE FUNCTION AND OXIDATIVE-METABOLISM IN POSTISCHEMIC MYOCARDIUM - ATTENUATION BY RUTHENIUM RED ADMINISTERED DURING REPERFUSION
DISSOCIATION BETWEEN CONTRACTILE FUNCTION AND OXIDATIVE-METABOLISM IN POSTISCHEMIC MYOCARDIUM - ATTENUATION BY RUTHENIUM RED ADMINISTERED DURING REPERFUSION
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DOI：
10.1161/01.res.71.3.567
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发表时间：
1992-09-01
影响因子：
20.1
通讯作者：
LERCH, R
中科院分区：
文献类型：
--
作者：
BENZI, RH;LERCH, R
与缺血后再灌注心肌的收缩功能相比，氧化代谢率可能不成比例地高。为了研究细胞内钙转运在再灌注后高能量消耗中的潜在参与，我们在离体大鼠心脏中测定了钌红（线粒体钙转运抑制剂）对收缩功能和氧化代谢率恢复的影响。经受 60 分钟无血流缺血的心脏在再灌注开始后 15 分钟时表现出左心室压力发展恢复不良，仅为对照心脏中测量的相应值的 7%（p < 0.01）。然而，心肌耗氧量恢复至对照的 84% (p = NS)。等容收缩性能（表示为心率和左心室压力发展的乘积）与心肌耗氧量的比率严重降低至对照的 6%（p < 0.01）。在再灌注最初 40 分钟内补充 6-mu-M 钌红的灌注液导致心肌耗氧量减少至再灌注 15 分钟后测量值的 65%（p < 0.01），尽管左心室压力增加了三倍（p < 0.05）。钌红将棕榈酸酯和葡萄糖的氧化减少到相当程度。在钌红输注期间，收缩性能与心肌耗氧量的比率逐渐增加，并且在再灌注30分钟后与对照心脏没有进一步差异。在用含钌红介质再灌注的心脏中，肌酸激酶的累积心肌释放减少了 47% (p < 0.05)。这些结果为以下假设提供了间接证据：细胞内钙转运增加的能量消耗可能涉及缺血后再灌注早期左心室性能与心肌氧化代谢率之间分离的机制。
The oxidative metabolic rate may be disproportionately high compared with contractile function in postischemic reperfused myocardium. To study the potential involvement of intracellular calcium transport in high energy expenditure after reperfusion, we determined in isolated rat hearts the effect of ruthenium red, an inhibitor of mitochondrial calcium transport, on recovery of contractile function and oxidative metabolic rate. Hearts subjected to 60 minutes of no-flow ischemia exhibited, at 15 minutes after the onset of reperfusion, poor recovery of left ventricular pressure development to only 7% of the corresponding value measured in control hearts (p < 0.01). However, myocardial oxygen consumption was recovered to 84% of control (p = NS). The ratio of isovolumic contractile performance (expressed as the product of heart rate and left ventricular pressure development) to myocardial oxygen consumption was severely depressed to 6% of control (p < 0.01). Supplementation of the perfusate with 6-mu-M ruthenium red during the initial 40 minutes of reperfusion resulted in a reduction of myocardial oxygen consumption to 65% of the value measured after 15 minutes of reperfusion in hearts reperfused without ruthenium red (p < 0.01), despite a threefold increase of left ventricular pressure development (p < 0.05). Oxidation of both palmitate and glucose was reduced to a comparable extent by ruthenium red. The ratio of contractile performance to myocardial oxygen consumption increased progressively during infusion of ruthenium red and did not differ further from control hearts after 30 minutes of reperfusion. Cumulative myocardial release of creatine kinase was reduced by 47% (p < 0.05) in hearts reperfused with ruthenium red-containing medium. The results provide circumstantial evidence for the hypothesis suggesting that enhanced energy expenditure by intracellular calcium transport may be involved in the mechanisms underlying the dissociation between left ventricular performance and myocardial oxidative metabolic rate early after postischemic reperfusion.