Brain energy metabolism in anesthetized rats in acute anemia.

In order to evaluate if pronounced anemic hypoxia gives rise to signs of cerebral oxygen lack the blood hemoglobin content was reduced to 6 and 3 g-(100 ml)(-1). Cerebral blood flow increased in spite of the fact that there was a moderate reduction in blood pressure, and in mean tissue CO2 tension, and in the absence of signs of an increased glyolytic rate in the tissue. With a reduction in a hemoglobin content to 3 g-(100 ml)(-1) there was a moderate increase in tissue lactate content and associated changes in other carbohydrate metabolites and in amino acids of the type seen in hypoxic hypoxia, suggesting that tissue hypoxia was present. However, since the concentrations of phosphocreatine and adenine nucleotides remained constant this hypoxia must have been slight. It is concluded that there is cerebral vasodilation in the brain in pronounced anemic hypoxia, and that this vasodilatation, in combination with the reduced viscosity, creates favourable conditions for cerebral oxygenation.