Figure 1.
Figure 1. Lack of histologic evidence of thrombosis or emboli in any organ despite a hematocrit value of 0.85. Reticulocyte numbers (A) were increased in erythropoietin transgenic mice, most prominently in the first 4 months (n = 5 per group). Time course of the hematocrit value (B) shows a plateau of 0.85 from 2 months onward in transgenic mice (n = 30 per group). BV indicates bronchial vein; wt, wild-type; tg, transgenic. *P < .01, #P < .001, compared with age-matched wild-type controls. Tissue sections from the lung and the heart of 8-month-old mice (C,E, wild-type mice; D,F, transgenic mice) demonstrate the plethora of erythrocytes in the vasculature of transgenic mice without signs of thrombosis or emboli. Original magnification, × 200 for panels C and D, trichrome, scale bar 50 μm. Original magnification, × 400 for panels E and F, hematoxylin and eosin, scale bar 20 μm.

Lack of histologic evidence of thrombosis or emboli in any organ despite a hematocrit value of 0.85. Reticulocyte numbers (A) were increased in erythropoietin transgenic mice, most prominently in the first 4 months (n = 5 per group). Time course of the hematocrit value (B) shows a plateau of 0.85 from 2 months onward in transgenic mice (n = 30 per group). BV indicates bronchial vein; wt, wild-type; tg, transgenic. *P < .01, #P < .001, compared with age-matched wild-type controls. Tissue sections from the lung and the heart of 8-month-old mice (C,E, wild-type mice; D,F, transgenic mice) demonstrate the plethora of erythrocytes in the vasculature of transgenic mice without signs of thrombosis or emboli. Original magnification, × 200 for panels C and D, trichrome, scale bar 50 μm. Original magnification, × 400 for panels E and F, hematoxylin and eosin, scale bar 20 μm.

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