Fructose 1,6-diphosphate administration attenuates post-ischemic ventricular dysfunction.
Fructose 1,6-diphosphate administration attenuates post-ischemic ventricular dysfunction.
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DOI：
10.1016/j.hlc.2005.12.004
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发表时间：
2006-04-01
期刊：
影响因子：
--
通讯作者：
Woo, Y Joseph
中科院分区：
文献类型：
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作者：
Cohen, Jeffrey E;Atluri, Pavan;Woo, Y Joseph
背景：心肌细胞在缺血时的能量产生依赖于无氧糖酵解，每葡萄糖产生两个三磷酸腺苷。用1，6-二磷酸果糖(FDP)增强底物可以绕过葡萄糖和磷酸果糖激酶消耗ATP的步骤，从而为每个FDP产生四个ATP。方法：雄性Wistar大鼠250~300g，结扎冠状动脉左前降支30min，再灌流30min。在缺血和再灌流之前，动物立即接受静脉推注FDP或生理盐水对照。再灌流30min后，用左室腔内压/容量电导微导管评价心肌功能。结果：与对照组(n=8)相比，fdp组(n=8)的左心室最大压力显著提高(100.5±5.4mmHgvs.69.1+/-1.9mmHgvs69.1+/-1.9mmHgvs69.1+/-1.9mmHgvs69.1+-1.9mmHgvs69.1+-1.9mmHgvs69.1+-1.9mmHgvs69.1+-1.9mmHg；p
BACKGROUND: Cardiomyocyte energy production during ischemia depends upon anaerobic glycolysis inefficiently yielding two ATP per glucose. Substrate augmentation with fructose 1,6-diphosphate (FDP) bypasses the ATP consuming steps of glucokinase and phosphofructokinase thus yielding four ATP per FDP. This study evaluated the impact of FDP administration on myocardial function after acute ischemia.METHODS: Male Wistar rats, 250-300 g, underwent 30 min occlusion of the left anterior descending coronary artery followed by 30 min reperfusion. Immediately prior to both ischemia and reperfusion, animals received an intravenous bolus of FDP or saline control. After 30 min reperfusion, myocardial function was evaluated with a left ventricular intracavitary pressure/volume conductance microcatheter. For bioenergetics studies, myocardium was isolated at 5 min of ischemia and assayed for ATP levels.RESULTS: Compared to controls (n=8), FDP animals (n=8) demonstrated significantly improved maximal left ventricular pressure (100.5+/-5.4 mmHg versus 69.1+/-1.9 mmHg; p