Abstract

A complex relationship exists between venous hemoglobin level and thrombosis risk. The hemoglobin content of capillary blood varies in healthy individuals in relation to that of venous blood with sex, age, season of the year, and venous hemoglobin level. (Murphy WG, et al. Blood 2010;116:2861-2). To study further the dynamics of this relationship, venous and capillary (finger pulp blood) hemoglobin levels were compared in 462 frequent blood donors with hereditary hemochromatosis. A linear mixed effects model was fitted to compare capillary hemoglobin with the difference between the venous and capillary hemoglobin. Random slopes and intercepts for each donor were modelled to account for inter-individual variability. A linear mixed effects model was fitted to hemoglobin levels over cumulative time since first donation for each person in separate analyses for capillary and venous hemoglobin levels. Random intercepts and random slopes were modelled within individuals. For each change of 1g/dL in capillary hemoglobin, the difference between venous and capillary hemoglobin changed by -0.694 g/dL, significantly different from zero (p<0.001), indicating a dynamic relationship between the two compartments. After venesection capillary hemoglobin rose by a mean of 0.496 mg/dL/day, (p<0.001) and venous hemoglobin by 0.113 mg/dL/day (p=0.019). The recovery rate for capillary hemoglobin between venesections was 4.39 times faster than for venous hemoglobin [t(4798)=2.743; p=0.006]. These data indicate that healthy individuals preserve venous hemoglobin at the expense of capillary hemoglobin as the red cell mass rises and falls, and that the capillary space buffers the venous hemoglobin level from changes in red cell mass. Since this space occupies > 10% of the intravascular volume (Chaplin H, et al. JCI 1953:32;1309-16) we estimate that 27% or more of a decrease or increase in red cell mass is accommodated by changes in hemoglobin level of capillary blood relative to the venous hemoglobin level. The mechanisms underlying these dynamics, such as NO-induced vasodilation by deoxyhemoglobin and modulation of the Fåhraeus effect, remain to be elucidated; however their implications for the relationship between hemoglobin level and thrombosis may be considerable.

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