S-nitroso Human Serum Albumin Attenuates Ischemia/Reperfusion Injury After Cardioplegic Arrest in Isolated Rabbit Hearts

Background Depletion of nitric oxide (NO) is associated with ischemia/reperfusion injury. The novel NO donor, S-nitroso human serum albumin (S-NO-HSA), could bridge NO depletion during reperfusion in cardiac transplantation and minimize ischemia/reperfusion injury. Methods In an isolated erythrocyte-perfused working heart model, rabbit hearts were randomly assigned after assessment of hemodynamic baseline values to receive S-NO-HSA (0.2 μmol/100 ml, n = 8), L-arginine (10 mmol/100 ml, n = 8) or albumin (control) (0.2 μmol/100 ml, n = 8). After 20 minutes of infusion, the hearts were arrested and stored in Celsior (4°C) enriched with respective drugs for 6 hours, followed by 75 minutes of reperfusion. Hemodynamic values were assessed and biopsy specimens were taken to determine calcium-ionophore stimulated release of NO and superoxide. Results During early reperfusion, recovery of cardiac output (75% ± 6% vs 49% ± 5%, p p p p p p p Conclusion S-NO-HSA improved hemodynamic functions after prolonged hypothermic cardiac arrest by supplementing NO and thereby decreasing ischemia/reperfusion injury.