Whitman G J, Niibori K, Yokoyama H, Crestanello J A, Lingle D M, Momeni R
Division of Cardiothoracic Surgery, Allegheny University Hospitals, Philadelphia, PA 19129, USA.
Mol Aspects Med. 1997;18 Suppl:S195-203. doi: 10.1016/s0098-2997(97)00017-4.
It has been hypothesized that CoQ10 (CoQ) pretreatment protects myocardium from ischemia reperfusion (I/R) injury by its ability to increase aerobic energy production as well as its activity as an antioxidant. Isolated hearts from rats pretreated with either CoQ 20 mg/kg i.m. and 10 mg/kg i.p. or vehicle 24 and 2 h prior to the experiment, were subjected to 15 min of equilibration (EQ), 25 min of ischemia, and 40 min of reperfusion (RP). Developed pressure, +/-dp/dt, myocardial oxygen consumption, and myocardial aerobic efficiency (DP/MVO2) were measured. 31P NMR spectroscopy was used to determine ATP and PCr concentrations. Lucigenin-enhanced chemiluminescence of the coronary sinus effluent was utilized to determine oxidative stress through the protocol. CoQ pretreatment improved myocardial function after ischemia reperfusion. CoQ pretreatment improved tolerance to myocardial ischemia reperfusion injury by its ability to increase aerobic energy production, and by preserving myocardial aerobic efficiency during reperfusion. Furthermore, the oxidative burst during RP was diminished with CoQ. Similarly it was hypothesized that CoQ protected coronary vascular reactivity after I/R via an antioxidant mechanism. Utilizing a newly developed lyposomal CoQ preparation given i.v. 15 min prior to ischemia, ischemia reperfusion was carried out on Langendorff apparatus as previously described. Just prior to ischemia and after RP, hearts were challenged with bradykinin (BK) and sodium nitroprusside (SNP) and change in coronary flow was measured. CoQ pretreatment protected endothelial-dependent and endothelial-independent vasodilation after I/R. We conclude that CoQ pretreatment protects coronary vascular reactivity after I/R via OH radical scavenger action.
有人提出假设，辅酶Q10（CoQ）预处理可通过增加有氧能量产生的能力及其作为抗氧化剂的活性来保护心肌免受缺血再灌注（I/R）损伤。在实验前24小时和2小时，分别用20mg/kg的CoQ进行肌肉注射和10mg/kg的CoQ进行腹腔注射预处理大鼠，或用赋形剂预处理大鼠，然后将分离的心脏进行15分钟的平衡（EQ）、25分钟的缺血和40分钟的再灌注（RP）。测量心脏的发展压力、±dp/dt、心肌耗氧量和心肌有氧效率（DP/MVO2）。用31P核磁共振波谱法测定ATP和磷酸肌酸（PCr）的浓度。利用鲁米诺增强的冠状窦流出液化学发光法通过该方案测定氧化应激。CoQ预处理改善了缺血再灌注后的心肌功能。CoQ预处理通过增加有氧能量产生的能力以及在再灌注期间保持心肌有氧效率，提高了对心肌缺血再灌注损伤的耐受性。此外，CoQ减少了再灌注期间的氧化爆发。同样有人提出假设，CoQ通过抗氧化机制保护I/R后的冠状血管反应性。在缺血前15分钟静脉注射新开发的脂质体CoQ制剂，然后在Langendorff装置上进行如前所述的缺血再灌注。就在缺血前和再灌注后，用缓激肽（BK）和硝普钠（SNP）刺激心脏，并测量冠状动脉流量的变化。CoQ预处理保护了I/R后的内皮依赖性和非内皮依赖性血管舒张。我们得出结论，CoQ预处理通过清除OH自由基的作用保护I/R后的冠状血管反应性。
