Lopez Marcos G, Pretorius Mias, Shotwell Matthew S, Deegan Robert, Eagle Susan S, Bennett Jeremy M, Sileshi Bantayehu, Liang Yafen, Gelfand Brian J, Kingeter Adam J, Siegrist Kara K, Lombard Frederick W, Richburg Tiffany M, Fornero Dane A, Shaw Andrew D, Hernandez Antonio, Billings Frederic T
Division of Anesthesiology Critical Care Medicine, Department of Anesthesiology, Vanderbilt University Medical Center, 1211 21st Avenue South, Suite 526, Nashville, TN, 37212, USA.
Division of Cardiothoracic Anesthesiology, Department of Anesthesiology, Vanderbilt University Medical Center, 1211 21st Avenue South, Suite 526, Nashville, TN, 37212, USA.
Trials. 2017 Jun 26;18(1):295. doi: 10.1186/s13063-017-2021-5.
Anesthesiologists administer excess supplemental oxygen (hyper-oxygenation) to patients during surgery to avoid hypoxia. Hyper-oxygenation, however, may increase the generation of reactive oxygen species and cause oxidative damage. In cardiac surgery, increased oxidative damage has been associated with postoperative kidney and brain injury. We hypothesize that maintenance of normoxia during cardiac surgery (physiologic oxygenation) decreases kidney injury and oxidative damage compared to hyper-oxygenation.
METHODS/DESIGN: The Risk of Oxygen during Cardiac Surgery (ROCS) trial will randomly assign 200 cardiac surgery patients to receive physiologic oxygenation, defined as the lowest fraction of inspired oxygen (FIO) necessary to maintain an arterial hemoglobin saturation of 95 to 97%, or hyper-oxygenation (FIO = 1.0) during surgery. The primary clinical endpoint is serum creatinine change from baseline to postoperative day 2, and the primary mechanism endpoint is change in plasma concentrations of F-isoprostanes and isofurans. Secondary endpoints include superoxide production, clinical delirium, myocardial injury, and length of stay. An endothelial function substudy will examine the effects of oxygen treatment and oxidative stress on endothelial function, measured using flow mediated dilation, peripheral arterial tonometry, and wire tension myography of epicardial fat arterioles.
The ROCS trial will test the hypothesis that intraoperative physiologic oxygenation decreases oxidative damage and organ injury compared to hyper-oxygenation in patients undergoing cardiac surgery.
ClinicalTrials.gov, ID: NCT02361944 . Registered on the 30th of January 2015.
麻醉医生在手术期间给患者输注过量的补充氧气（高氧）以避免缺氧。然而，高氧可能会增加活性氧的产生并导致氧化损伤。在心脏手术中，氧化损伤增加与术后肾脏和脑损伤有关。我们假设，与高氧相比，心脏手术期间维持正常氧合（生理氧合）可减少肾脏损伤和氧化损伤。
方法/设计：心脏手术期间氧风险（ROCS）试验将随机分配200名心脏手术患者，使其在手术期间接受生理氧合（定义为维持动脉血红蛋白饱和度在95%至97%所需的最低吸入氧分数（FIO））或高氧（FIO = 1.0）。主要临床终点是从基线到术后第2天的血清肌酐变化，主要机制终点是血浆中F-异前列腺素和异呋喃浓度的变化。次要终点包括超氧化物生成、临床谵妄、心肌损伤和住院时间。一项内皮功能子研究将使用血流介导的血管舒张、外周动脉张力测量法以及心外膜脂肪小动脉的线张力肌电图来研究氧治疗和氧化应激对内皮功能的影响。
ROCS试验将检验以下假设：与接受高氧的心脏手术患者相比，术中生理氧合可减少氧化损伤和器官损伤。
ClinicalTrials.gov，标识符：NCT02361944。于2015年1月30日注册。
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