Previous studies have concluded that
polycythemia decreases
oxygen delivery primarily because of a large fall in cardiac output associated with a rise in systemic vascular resistance that has been attributed to increased blood viscosity. However, because other studies have shown that
polycythemia may not reduce
oxygen delivery, an alternative hypothesis is that cardiac output falls in response to a rising
oxygen content, thereby maintaining
oxygen delivery constant. To determine whether
oxygen content participates in the regulation of cardiac output during
polycythemia, we studied eight chronically instrumented dogs trained to exercise on a treadmill. The dogs underwent exchange transfusion with packed red blood cells containing
methemoglobin, which caused an increase in hematocrit from 35 +/- 1 to 50 +/- 1% and in viscosity, with little change in
oxygen content. The expected fall in exercise cardiac output failed to occur after exchange transfusion with red blood cells containing
methemoglobin (7.5 +/- 4 vs. 6.8 +/- 0.5 l/min; P = not significant), and there was no rise in systemic vascular resistance.
Methylene blue was then administered intravenously to facilitate conversion of
methemoglobin to
oxyhemoglobin, which increased
oxygen content (12.8 +/- 0.9 vs. 18.4 +/- 0.9 vol%; P < 0.01) with no change in hematocrit or viscosity. Resting cardiac output did not change significantly, but there was a significant decrease in exercise output (6.8 +/- 0.5 vs. 5.8 +/- 0.4 l/min; P < 0.05). Thus we conclude that the fall in cardiac output seen in acute
polycythemia results in part from the regulation of
oxygen delivery and is not due solely to increased blood viscosity.