Post-irradiation anemia is primarily the consequence of red cell aplasia and of hemorrhage secondary to thrombocytopenia. Data have been presented which indicate that in addition there is intravascular red cell damage. Of particular interest was the observation herein presented that the damage to the red cells produced by ionizing radiations is of an indirect nature. Using the chromium technic it was possible to demonstrate red cell damage as early as the 1st-3rd post-irradiation day. In these studies tagged cells were transfused 15-55 days prior to irradiation in order to establish the elution rate of Cr51. On the 1st-3rd day following irradiation there was an abrupt increase in the rate of Cr51 loss. When normal cells were transfused immediately after irradiation there was also a striking increase in the rate of Cr51 loss above that observed in normal animals, indicating that radiation damage to the red cell was indirect. When cells were transfused from irradiated donors into normal recipients, it was not possible to demonstrate red cell damage prior to the 10th post-irradiation day, indicating that the damage was progressive.

Since there was a selective loss of Cr51 it is suggested that chromium produced an additive damage to the cell. The possible implication of this observation in the use and interpretation of Cr51 survival curves is discussed.

It was also determined that red cells which were recirculated following extravasation during the thrombocytopenic phase of radiation injury had a shortened survival, whereas normal cells, tagged and injected intramuscularly into normal recipients survived normally on return to the general circulation. Cells collected from dogs one day after irradiation, tagged with Cr51 and then injected intramuscularly into normal recipients, showed a striking increase in the rate of destruction. Cells collected on the 4th post-irradiation day were destroyed even more rapidly. These studies confirmed the early onset of radiation injury to the cells, its progressive nature, and demonstrated the damage incurred as a result of passage through the extravascular cycle. As might be expected there was also a shortened survival of red cells collected from the thoracic lymph of thrombopenic irradiated animals.

Conclusions: 1. Ionizing radiations produce intravascular red cell damage in addition to the known loss incident to hemorrhage. This damage is evident within 24-72 hrs. of irradiation.

2. The red cell damage is an indirect and progressive effect of irradiation.

3. Those cells which are returned to the general circulation, following passage through an extravascular cycle, are damaged. The extent of injury to normal cells is such that it is not detectable by current methods. However, the addition of a second injury, such as that following irradiation, enables the detection of this damage.

4. Chromium "elution" is altered by irradiation injury.

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