Hemolysis compromises nitric oxide-dependent vasodilatory responses in patients undergoing major cardiovascular surgery.

Background: The hemolytic products cell-free oxyhemoglobin (FHb) and arginase-1 reduce nitric oxide (NO) bioavailability by scavenging NO and by degrading the NO precursor arginine to ornithine, respectively. In this study we evaluated the relevance of hemolysis to NO-dependent blood flow in patients undergoing cardiovascular surgery.
Methods: Plasma FHb, arginase-1, and amino acid concentrations were measured perioperatively. Forearm blood flow (FBF) responses to the intra-arterial administered NO-donor sodium nitroprusside (SNP) and the endothelium-dependent vasodilator acetylcholine (ACh) were measured by venous occlusion plethysmography.
Results: When peak values plasma FHb and arginase-1 were found, vascular dilatation to SNP, but not ACh, was significantly reduced compared with 1 day postoperatively, when FHb had returned to baseline levels (p < 0.05). Interestingly, plasma FHb concentration was inversely correlated to FBF responses to SNP (r -0.93, p < 0.001). In contrast, the increase in arginase-1 was not biologically relevant as the ratio of plasma arginine to ornithine remained constant.
Conclusion: We conclude that hemolysis with concomitant release of FHb during cardiovascular surgery is associated with impaired NO-dependent forearm blood flow.
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