Objectives: The aim of this pilot study was to elucidate the effects of exogenous nitric oxide (NO) supply to the extracorporeal circulation circuit for cardioprotection against ischemia-reperfusion injury during coronary artery bypass grafting (CABG) with cardiopulmonary bypass (CPB).Methods: A total of 60 patients with coronary artery disease scheduled for CABG with CPB were enrolled in a prospective randomized study. Patients were allocated randomly to receive treatment according to standard or modified CPB protocol where 40-ppm NO was added to the CPB circuit during cardiac surgery. The primary endpoint was the measurement of cardiac troponin I (cTnI). The secondary end points consisted in the measurements of creatine kinase-muscle/brain fraction (CK-MB) and vasoactive inotropic score (VIS).Results: NO delivered into the CPB circuit had a cardioprotective effect. The level of cTnI was significantly lower in NO-treated group compared with the control group 6 hours after surgery: 1.79 AE 0.39 ng/mL versus 2.41 AE 0.55 ng/mL, respectively (P ¼ .001). The CK-MB value was significantly lower in NOtreated group compared with the control group 24 hours after surgery: 47.

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Introduction: Acute kidney injury (AKI) is a serious complication of cardiac surgery with cardiopulmonary bypass (CPB). Postoperative AKI develops in 30% to 52% of cardiac surgery patients and 2% to 5% of these patients require renal replacement therapy. Hypothesis: We hypothesized that nitric oxide treatment during cardiac surgery with CPB can decrease AKI incidence in adult patients. The aim of study was to evaluate the effects of nitric oxide supplementation to CPB circuit on the development of cardiac surgery-associated AKI. Methods: A prospective randomized controlled study included 96 patients with moderate risk of renal complications who underwent elective cardiac surgery with CPB. The study protocol was registered at www.clinicaltrials.gov (#NCT03527381). Patients were randomly assigned to either the nitric oxide supplementation to CPB circuit (NO-treatment group, n = 48) or the usual care (control group, n = 48). 40-ppm nitric oxide was administered in NO-treatment group during the entire CPB period. The primary outcome was AKI incidence. Results: Nitric oxide treatment was associated with a significant decrease in AKI incidence (10 (20.8%) versus 20 (41.6%); RR 0.5 (95% CI 0.26-0.95; p =0.023) and a higher urine output during CPB (2.6 [2.1;5.08] versus 1.7 [0.80;2.50] mL/kg/h; p = 0.0002). Urinary neutrophil gelatinase-associated lipocalin levels were significantly lower in NO-treatment group 4 h after surgery: 1.12 [0.75;5.8] versus 4.62 [2.02;34.55] ng/mL; p = 0.005. Concentrations of nitric oxide metabolites in NO-treatment group significantly increased at 5 min post-clamping, 5 min after declamping, and at the end of surgery. The concentrations of proinflammatory and anti-inflammatory mediators and free plasma hemoglobin did not significantly differ between groups. Conclusions: Nitric oxide administration to patients at moderate risk of renal complications undergoing elective cardiac surgery with CPB was associated with a decrease in AKI incidence. The implications of study for clinical practice expand the array of methods, which may be used for prevention of AKI in cardiac surgery patients.

A hypoxic–hyperoxic preconditioning (HHP) may be associated with cardioprotection by reducing endothelial damage and a beneficial effect on postoperative outcome in patients undergoing cardiac surgery with cardiopulmonary bypass (CPB). Patients (n = 120) were randomly assigned to an HHP and a control group. A safe, inhaled oxygen fraction for the hypoxic preconditioning phase (10–14% oxygen for 10 min) was determined by measuring the anaerobic threshold. At the hyperoxic phase, a 75–80% oxygen fraction was used for 30 min. The cumulative frequency of postoperative complications was 14 (23.3%) in the HHP vs. 23 (41.1%), p = 0.041. The nitrate decreased after surgery by up to 20% in the HHP group and up to 38% in the control group. Endothelin-1 and nitric oxide metabolites were stable in HHP but remained low for more than 24 h in the control group. The endothelial damage markers appeared to be predictors of postoperative complications. The HHP with individual parameters based on the anaerobic threshold is a safe procedure, and it can reduce the frequency of postoperative complications. The endothelial damage markers appeared to be predictors of postoperative complications.

Background: The hypothesis is that a hypoxic-hyperoxic preconditioning (HHP) is associated with a protective effect on myocardial function by reducing endothelial damage and a beneficial effect on postoperative outcome in patients undergoing cardiac surgery with cardiopulmonary bypass (CPB). Methods: Patients (n=120) were randomly assigned to an HHP and a control group. A safe inhaled oxygen fraction for the hypoxic preconditioning phase (10-14% oxygen for 10 minutes) was determined by measuring the anaerobic threshold. At hyperoxic phase, 75-80% oxygen fraction was used during 30 minutes. Results: The cumulative frequency of postoperative complications was 14 (23.3%) in the HHP vs 23 (41.1%), p=0.041. The nitrate decreased after surgery by up to 20% in the HHP group and up to 38% in the control group. Endothelin-1 and nitric oxide metabolites were stable in HHP but remained low more than 24 h in control group. The endothelial damage markers appeared to be predictors of postoperative complications. Conclusion: The HHP with individual parameters based on the anaerobic threshold is a safe procedure, it can reduce the frequency of postoperative complications. The endothelial damage markers appeared to be predictors of postoperative complications.