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Relationship between absolute and relative hematocrit changes and bone marrow response in rats
1Department of Physiology, Faculty of Medicine, Thracian University, Stara Zagora.
Abstract:
The object of the present study was to evaluate the physiologic mechanisms regulating erythropoiesis by monitoring the changes in reticulocyte count in the circulation and the formation of erythroblastic islands in the bone marrow following hypertransfusion and dehydration. Forty-eight male Wistar rats (110-130 grams) were transfused with 70% isogenic suspension of washed and packed red cells at a dose of 2.5 ml/100 g body weight intravenously on two consecutive days (absolute erythrocytosis) or deprived of water for three days to produce relative erythrocytosis and then injected i.v. with saline at a dose of 2.5 ml/100 g body weight with water provided at libitum. Hematocrit was measured using the microhematocrit method. Reticulocytes were enumerated using the new methylene blue stain. Plasma EPO levels were measured radioimmunologically and a bone marrow suspension was prepared for morphological examination and absolute erythroblastic islands determination. We observed a marked suppression of erythropoiesis following the transfusion as evidenced by the elevation in hematocrit values up to 0.64 +/- 0.04, a decrease in reticulocyte count and plasma EPO reduction--13.5 +/- 3.4 mU/ml (P < 0.05) and a suppression of EO formation in the bone marrow (P < 0.01). The hematocrit of the dehydrated rats was elevated during the first 24 hours (P < 0.001). Reticulocytes, as well as EO, decreased on day 3 down do 53.6 x 10(9)/l +/- 9.8 x 10(9)/l (P < 0.001) and 153.6 x 10(3) +/- 21.5 x 10(3)/femur (P < 0.001), respectively. The EPO level was measured simultaneously--16.3 +/- 4.2 mU/ml versus 24.6 +/- 5.3 mU/ml at day 1 (P < 0.001). Following rehydration, a fast increase in the hematocrit value with a concomitant increase in EO and the reticulocyte counts was observed. Our results show that the absolute and relative changes in hematocrit values are paramount in the feedback mechanism for erythroid homeostasis.