Motl Jill, Radhakrishnan Jeejabai, Ayoub Iyad M, Grmec Stefek, Gazmuri Raúl J
1Resuscitation Institute at Rosalind Franklin University, Chicago, IL; 2Center for Emergency Medicine Maribor, Faculty of Medicine and Faculty of Health Sciences, University of Maribor, Maribor, Slovenia; 3Faculty of Medicine, University of Ljubljana; 4Intensive Care Unit, University Clinical Center Maribor, Maribor, Slovenia; 5Departments of Medicine and Physiology & Biophysics, Rosalind Franklin University; and 6Critical Care Medicine, Captain James A. Lovell Federal Health Care Center, Chicago, IL.
Am J Ther. 2014 Sep-Oct;21(5):352-7. doi: 10.1097/MJT.0b013e31824e2b9f.
Resuscitation from cardiac arrest is partly limited by progressive reduction in left ventricular distensibility, leading to decreased hemodynamic efficacy of cardiopulmonary resuscitation (CPR). Reduction in left ventricular distensibility has been linked to loss of mitochondrial bioenergetic function that can result from oxidative injury. Attenuation of oxidative injury by administration of vitamin C during CPR may help maintain left ventricular distensibility and favor resuscitability and survival. Ventricular fibrillation was electrically induced in 2 series of 16 rats each and left untreated for 10 minutes. Resuscitation was attempted by 8 minutes of CPR and delivery of electrical shocks. Dehydroascorbate (DHA)-an oxidized form of vitamin C that enters the cell via glucose transporters-was used in series 1 and ascorbic acid (AA)-the reduced form of vitamin C that enters the cell via specialized AA transporters-in series 2. In each series, rats were randomized 1:1 to receive a 250 mg/kg right atrial bolus of DHA or AA or vehicle immediately before chest compression. Left ventricular distensibility-measured as the ratio between coronary perfusion pressure and compression depth-was numerically lower (not significant) in rats that received DHA (1.6 ± 0.2 vs. 1.9 ± 0.7 mm Hg/mm) and AA (1.8 ± 0.6 vs. 1.9 ± 0.3 mm Hg/mm). In addition, resuscitability was compromised by DHA (2/8 vs. 7/8; P = 0.041) and by AA (0/8 vs. 5/8; P = 0.026). AA levels in mitochondria were no different than control. Vitamin C failed to preserve left ventricular distensibility during CPR and had detrimental effects on resuscitability, suggesting possible disruption of protective signaling mechanisms during oxidative stress by vitamin C.
心脏骤停复苏受到左心室扩张性逐渐降低的部分限制，导致心肺复苏（CPR）的血流动力学效果下降。左心室扩张性降低与氧化损伤导致的线粒体生物能量功能丧失有关。在CPR期间给予维生素C减轻氧化损伤可能有助于维持左心室扩张性，并有利于复苏和存活。在两组各16只大鼠中电诱导室颤，并使其未经治疗持续10分钟。尝试通过8分钟的CPR和电击进行复苏。在第1组中使用脱氢抗坏血酸（DHA）——维生素C的氧化形式，通过葡萄糖转运体进入细胞，在第2组中使用抗坏血酸（AA）——维生素C的还原形式，通过专门的AA转运体进入细胞。在每组中，大鼠按1:1随机分组，在胸部按压前立即接受250mg/kg右心房推注DHA或AA或赋形剂。以冠状动脉灌注压与按压深度之比衡量的左心室扩张性，在接受DHA的大鼠中数值较低（无统计学意义）（1.6±0.2 vs. 1.9±0.7mmHg/mm），在接受AA的大鼠中也是如此（1.8±0.6 vs. 1.9±0.3mmHg/mm）。此外，DHA（2/8 vs. 7/8；P = 0.041）和AA（0/8 vs. 5/8；P = 0.026）均损害了复苏能力。线粒体中的AA水平与对照组无差异。维生素C在CPR期间未能维持左心室扩张性，并且对复苏能力有不利影响，提示维生素C可能在氧化应激期间破坏了保护性信号机制。
