Blood transfusions may impair endothelium-dependent vasodilatation during coronary artery bypass surgery

- Intraoperative blood transfusions produce a 2.4 fold higher fHb concentration compared to pre-transfusion level
- High fHb concentrations impair endothelium-dependent relaxation through NO scavenging in CABG patients
- These findings obtained in vitro and in vivo suggest caution for using vasopressive agents in patients with substantial transfusion requirements

ObjectiveThe hemolytic product free-hemoglobin (fHb) reduces nitric oxide (NO) bioavailability. The present study aims to establish whether administration of different blood transfusions result in increased circulating fHb levels and NO consumption with effects on arterial NO-dependent blood flow in patients undergoing CABG surgery.MethodsNinety-five consecutive patients undergoing elective CABG surgery were prospectively divided in four groups based on blood transfusion requirements during surgery: stored blood cells (SBC, n. 21), intraoperative autologous salvaged blood (ASB, n. 25), SBC and ASB (n.22), no transfusion (control, n. 27).Blood samples were collected before and after intervention to analyse plasma levels of fHb and NO consumption. Endothelium-dependent relaxation was assessed in left internal mammary artery (LIMA) rings harvested before chest closure. Peripheral artery tonometry was assessed after intervention.ResultsTransfusions with SBC increased plasma fHb (p < 0.05). Transfusions of ASB resulted in higher plasma fHb compared to SBC (p < 0.01). fHb concentrations directly correlated with NO consumption (r = 0.65, p < 0.001). Maximal endothelium-dependent relaxation in LIMA was significantly attenuated in SBC and ASB patients compared to control (15.2 ± 3.1% vs 21.1 ± 2.5% vs 43 ± 5.0% respectively; p < 0.01). Significant correlations were identified between the aortic pressure wave velocity, plasma fHb concentration and NO consumption (p < 0.01).ConclusionsIntraoperative blood transfusions and particularly autologous salvaged blood impair endothelium-dependent relaxation through NO scavenging by fHb. These findings obtained in vitro and in vivo provide new insights into the adverse relation between blood transfusions and patient outcome.