Hemoglobinemia in mice exposed to high altitude

Male and female mice were exposed to a simulated altitude of 5,500m for 10, 30 or 90 days. After exposure to altitude for 90 days one group of each sex was then returned to sea level pressures for 10 days. In addition to the expected increases in hematocrit and hemoglobin, altitude exposure increased the 2,3-DPG content of red cells. Maximum values of 2,3-DPG (moles/g hemoglobin) occurred after 10 days at altitude and thereafter declined to values comparable to those in sea level mice despite continued exposure to hypoxia.As previously described for rats, mice also exhibit an altitude-induced hemoglobinemia which occurs in the face of a polycythemia. Plasma hemoglobin concentrations were at a steady state after about 30 days at altitude. Both sexes also showed a significant splenic hypertrophy, a bilirubinemia and a hemoglobinuria as a result of altitude exposure. As assessed in male mice a significant induction of heme oxygenase activity occurred in the kidneys but not in the spleen or liver. The latter finding contrasts with results previously observed in rats where induction of heme oxygenase occurs in the liver desplte a decrease in the liver/body weight ratio.Sex differences in the response to hypoxia previously observed with rats also occur in mice. The altitude-induced rise in hematocrit but not hemoglobin appears to be more pronounced in males as was the failure to gain weight. Perhaps both male mice and rats are more severely compromised by altitude than are females of the same speciesThe time course of the hemoglobinemia and its reversal at sea level paralleled the changes in hemoglobin and hematocrit suggesting that it was correlated with the demand on hematopoietic effort. Perhaps the hemoglobinemia is secondary to ineffective hematopoiesis.