The effects of diaspirin cross-linked hemoglobin on the tone of human saphenous vein.

Abstract

Diaspirin cross-linked hemoglobin (DCL-Hb), when infused into animals, causes vasoconstriction thought to be caused by nitric oxide (NO) binding by the hemoglobin molecule. The purpose of this study was to ascertain whether DCL-Hb causes vasoconstriction in human saphenous vein taken from patients undergoing myocardial revascularization and whether NO scavenging is the mechanism. The direct effect of DCL-Hb on saphenous vein tone was tested by adding increasing concentrations (10(-8) to 10(-5)M) of the drug. In an additional series of experiments, the influence of DCL-Hb on the dilator response to endothelial dependent and independent vasodilators was tested. This was achieved by attempting either to reverse the effects of acetylcholine, sodium nitroprusside, or S-nitrosylglutathione with prior incubation with DCL-Hb or to inhibit the dilator response in vessels preconstricted with 10(-6)M norepinephrine. There was no effect of DCL-Hb alone on saphenous vein tone. DCL-Hb significantly reduced vasodilatation with all vasodilators (P < 0.05). After maximal relaxation with sodium nitroprusside and s-nitrosylglutathione, there was significant vasoconstriction with DCL-Hb at concentrations larger than 10(-6)M, (P < 0.05). The authors conclude that DCL-Hb does not constrict human saphenous vein but can affect vessel tone by reversal of the effect of endogenously or exogenously released NO.