Horvath Katharina, Taschner Alexander, Adamowitsch Nikolas, Falkner von Sonnenburg Markus, Fleischmann Edith, Kabon Barbara, Fraunschiel Melanie, Reiterer Christian, Graf Alexandra
Department of Anaesthesia, General Intensive Care Medicine and Pain Medicine, Medical University of Vienna, 1090 Vienna, Austria.
IT Systems and Communications, Medical University of Vienna, 1090 Vienna, Austria.
J Clin Med. 2023 Feb 3;12(3):1222. doi: 10.3390/jcm12031222.
Increased von Willebrand Factor (vWF) activity mediates platelet adhesion and might be a contributor to the development of thrombotic complications after surgery. Although in vitro studies have shown that hyperoxia induces endovascular damage, the effect of perioperative supplemental oxygen as a possible trigger for increased vWF activity has not been investigated yet. We tested our primary hypothesis that the perioperative administration of 80% oxygen concentration increases postoperative vWF activity as compared to 30% oxygen concentration in patients at risk of cardiovascular complications undergoing major noncardiac surgery. A total of 260 patients were randomly assigned to receive 80% versus 30% oxygen throughout surgery and for two hours postoperatively. We assessed vWF activity and Ristocetin cofactor activity in all patients shortly before the induction of anesthesia, within two hours after surgery and on the first and third postoperative day. Patient characteristics were similar in both groups. We found no significant difference in vWF activity in the overall perioperative time course between both randomization groups. We observed significantly increased vWF activity in the overall study population throughout the postoperative time course. Perioperative supplemental oxygen showed no significant effect on postoperative vWF and Ristocetin cofactor activity in cardiac risk patients undergoing major noncardiac surgery. In conclusion, we found no significant influence of supplemental oxygen in patients undergoing major non-cardiac surgery on postoperative vWF activity and Ristocetin cofactor activity.
血管性血友病因子(vWF)活性增加介导血小板黏附,可能是术后血栓形成并发症发生的一个因素。尽管体外研究表明高氧会导致血管内损伤,但围手术期补充氧气作为vWF活性增加的可能诱因的作用尚未得到研究。我们检验了我们的主要假设,即在接受非心脏大手术且有心血管并发症风险的患者中,与30%氧气浓度相比,围手术期给予80%氧气浓度会增加术后vWF活性。总共260例患者被随机分配在整个手术过程及术后两小时接受80%或30%的氧气。我们在麻醉诱导前、术后两小时内以及术后第一天和第三天对所有患者评估vWF活性和瑞斯托霉素辅因子活性。两组患者的特征相似。我们发现在整个围手术期时间进程中,两个随机分组之间的vWF活性没有显著差异。我们观察到在整个术后时间进程中,总体研究人群的vWF活性显著增加。围手术期补充氧气对接受非心脏大手术且有心脏风险的患者术后vWF和瑞斯托霉素辅因子活性没有显著影响。总之,我们发现非心脏大手术患者补充氧气对术后vWF活性和瑞斯托霉素辅因子活性没有显著影响。