The hematology and biochemistry of canine postnatal anemia

In conclusion, postnatal changes in the 2,3-DPG concentration of the canine erythrocyte are directly related to changes in erythrocyte 1,3-diphosphoglycerate concentration. There is not apparent differential regulation of 2,3-DPG mutase or phosphatase activities. Glucose consumption and lactate production of the canine erythrocyte do not change during postnatal development, thus, overall rate controlling reactions in the upper portion of the glycolytic pathway do not regulate the changes in 1,3-diphosphoglycerate. The analysis of intermediate and enzyme levels below the 2,3-DPG shunt indicates that pyruvate kinase functions as a controlling sink reaction. Variation in the pyruvate kinase step causes changes in the erythrocyte phosphoenolpyruvate levels. Since the enolase, phosphoglyceromutase and phosphoglycerate kinase reactions are at equilibrium, changes in phosphoenolpyruvate concentrations are paralleled by changes in the concentrations of 1,3-diphosphoglycerate and 2,3-DPG. We propose that the rise in erythrocyte 2,3-DPG, during the first 60 days of postnatal age, results from a decline in the levels of the fetal or M2 isozyme of pyruvate kinase. The subsequent decline in erythrocyte 2,3-DPG to normal adult levels may result from a developmental change in pyruvate kinase isozymes. The changes in erythrocyte glycolysis following birth increase the oxygen transporting efficiency of hemoglobin at the higher oxygen tensions of the neonatal environment. This provides an initial reserve of blood oxygen transport capacity which suppresses erythrocyte production, resulting in the condition defined as postnatal anemia. There is no apparent defect in postnatal erythropoiesis.