The influence of acute normovolemic anemia on cerebral blood flow and oxygen consumption of anesthetized rats.

The influence of acute normovolemic anemia on cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRo2) was studied in normocapnic rats under nitrous oxide anaesthesia. The arterial hemoglobin content was reduced to values of about 12, 9, 6 and 3 g.(100 ml)(-1) by arterial bleeding and substitution with equal volumes of homolgous plasma. The CBF increased in proportion to the reduction in hemoglobin content to reach values of 500-600 per cent of normal at extreme degrees of anemia, but CMR02 remained unchanged. Cerebral venous PO2 and oxygen saturation did not decrease below normal values, indicating that tissue hypoxia did not develop. However, since the increase in CBF at hemoglobin concentrations of below 9 g(100 ml)(-1) was far in excess of that expected from the decrease in viscosity the results indicate thatdilatation of cerebral resistance vessels occurred. This dilatation, which was obviously related to the fall in arterial oxygen content, cannot be explained by any of the current theories proposed to explain cerebral hyperemia in hypoxia.