LAUSR

Hemolytic anemia is reduced blood oxygen-carrying capacity resulting from the depletion of red blood cells. Treatment for severe cases involves transfusion to improve oxygen delivery (DO2), which carries risk. In humans, a total hemoglobin (tHb) concentration of 8 g/dL is severe, and < 7 indicates transfusion. Some evidence suggests compensatory mechanisms maintaining DO2 are not compromised until < 5 g/dL rendering transfusion at 7 premature. A Sprague Dawley rat model of phenylhydrazine-induced HA was assessed over decreasing tHb for a DO2 decompensation point. Three groups (100, 50, or 25% tHb, equating to 16.4, 7.4, or 3.2 g/dL) were generated. Cardiopulmonary, blood chemistry and oxygenation parameters were measured under anethesia. Vasoconstrictive responsiveness to phenylephrine was assessed in the exteriorized spinotrapezius. For 50% tHb, cardiopulmonary parameters, DO2, and lactate were similar to 100%. Enhanced vasoconstriction occurred with 50% (p < 0.0001), not 25%. The 25% group showed decreases in cardiopulmonary parameters, DO2 and lactate compared to 100% and 50% (p < 0.05). DO2 showed a positive correlation with lactate at 25%, but decompensation, defined by peripheral hypoxia, was not reached. This is the first study relating DO2 to tHb in rats. A 50% reduction in tHb was supported by vascular compensation while 25% levied the cardiopulmonary system. A decompensation point was not identified. A rising need for treatment as tHb levels decline below 8 g/dL is evident, but, as compensatory mechanisms remain intact as tHb approaches 3.2 g/dL in rats, a transfusion limit of 5 g/dL in healthy patients is supported.