The role of RBC destruction in vascular regions with high turbulence on atherosclerosis.

After intravascular red blood cell (RBC) destruction, released hemoglobin exceeding the binding capacities of haptoglobin and hemopexin would contribute, as free hemoglobin and/or hemin and/or methemalbumin, to the pathogenesis of atherosclerosis. Especially in some regions of vasculature with a high turbulence strong enough to destruct fragile or old RBCs, free hemoglobin concentrations can exceed locally the binding capacities of haptoglobin and hemopexin although their measured venous concentrations are normal. As a very simple model of this possible very local event we analysed free hemoglobin and methemalbumin levels after blood collection into evacuated tubes, and found that the increase of methemalbumin is more significant than free hemoglobin. The measurement of free hemoglobin and methemalbumin concentrations of arterial blood samples just from pre- and post-atherosclerotic lesions can likely shed new light on our understanding of the development of atherosclerosis.