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Background: Elevated postoperative N-terminal pro-B-type natriuretic peptide (NT-proBNP) concentrations are predictive for cardiac adverse events in noncardiac surgery. Studies indicate that supplemental oxygen decreases sympathetic nerve activity and might, therefore, improve cardiovascular function. Thus, we will test the effect of perioperative supplemental oxygen administration on NT-proBNP release after surgery. Methods/design: We will conduct a single-center, double-blinded, randomized trial at the Medical University of Vienna, including 260 patients with increased cardiac risk factors undergoing moderate-to high-risk noncardiac surgery. Patients will be randomly assigned to receive 80% versus 30% oxygen during surgery and for 2 h postoperatively. The primary outcome will be the difference in maximum NT-proBNP release after surgery. As secondary outcomes we will assess the effect of supplemental oxygen on postoperative maximum troponin T concentration, oxidation-reduction potential, von Willebrand factor concentration and perioperative fluid requirements. We will perform outcome measurements 2 h after surgery, on postoperative day 1 and on postoperative day 3. The NT-proBNP concentration and the oxidation-reduction potential will also be measured within 72 h before discharge. Discussion: Our trial should determine whether perioperative supplemental oxygen administration will reduce the postoperative release of NT-proBNP in patients with preoperative increased cardiovascular risk factors undergoing noncardiac surgery. Trial registration: ClinicalTrials.gov, ID: NCT03366857. Registered on 8th December 2017.

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Renal transplantation is associated with ischemia/reperfusion (I/R) injury resulting in enhanced formation of reactive oxygen species (ROS), inflammation and activation of the innate immune system. [1][2][3] ROS production is mainly released from three different systems: the nicotinamide adenine dinucleotide phosphate oxidase system, nitric oxide synthase system, and xanthine oxidase system. [3][4][5][6] Ischemia induced adenosine tri-phosphate depletion leads to an increased hypoxanthine formation, which is converted to hydrogen peroxide (H 2 O 2 ) and superoxide (O − 2 ). 4,5 Specifically, activated endothelial cells in ischemic tissue are major contributor to an overwhelming ROS release. [6][7][8] Mannitol is an osmotic diuretic with proposed antioxidative capacity. Mannitol is commonly used in partial nephrectomy and renal transplantation to attenuate I/R injury. 9,10 However, there is only a small number of experimental animal studies evaluating the redox scavenging effects of mannitol. 11,12 Interestingly, a recent trial

Noncardiac surgery is associated with hemodynamic perturbations, fluid shifts and hypoxic events, causing stress responses. Copeptin is used to assess endogenous stress and predict myocardial injury. Myocardial injury is common after noncardiac surgery, and is often caused by myocardial oxygen demand-and-supply mismatch. In this secondary analysis, we included 173 patients at risk for cardiovascular complications undergoing moderate- to high-risk major abdominal surgery. Patients were randomly assigned to receive 80% or 30% oxygen throughout surgery and the first two postoperative hours. We evaluated the effect of supplemental oxygen on postoperative Copeptin concentrations. Copeptin concentrations were measured preoperatively, within two hours after surgery, on the first and third postoperative days. In total, 85 patients received 0.8 FiO2, and 88 patients received 0.3 FiO2. There was no significant difference in postoperative Copeptin concentrations between both study groups (p = 0.446). Copeptin increased significantly within two hours after surgery, compared with baseline in the overall study population (estimated effect: −241.7 pmol·L−1; 95% CI −264.4, −219.1; p < 0.001). Supplemental oxygen did not significantly attenuate postoperative Copeptin release. Copeptin concentrations showed a more immediate postoperative increase compared with previously established biomarkers. Nevertheless, Copeptin concentrations did not surpass Troponin T in early determination of patients at risk for developing myocardial injury after noncardiac surgery.