Effect of increased oxygen affinity and anemia on cardiac output and its distribution

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Abstract
Effect of increased blood O2 affinity on cardiac output and its distribution was studied in conscious sedated rats by the microsphere-reference sample method. After a preliminary measurement of cardiac output and its distribution, rats were exchange transfused with normal blood or low-P50 (PO2 at which hemoglobin is half-saturated with O2) blood; other groups were made anemic with and without a simultaneous reduction in P50. Reduction in P50 from 38 to 17 Torr did not change cardiac output, pulse, or blood pressure but caused, after allowance for changes in controls, a 102% increase in coronary blood flow and an 88% increase in cerebral blood flow. Anemia (hematocrit = 22%) produced similar changes in coronary and cerebral flow. When anemia was combined with a 12-Torr reduction in P50, coronary and cerebral flow increased by 297 and 209%, respectively. These increases in coronary and cerebral flow were not attributable to increased cardiac work or hypercapnia. It is concluded that a left shift of the O2 dissociation curve induces increased blood flow to brain and heart, probably in compensation for decreased tissue O2 pressure.