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

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.