Borgström L, Norberg K, Siesjö B K
Acta Physiol Scand. 1976 Apr;96(4):569-74. doi: 10.1111/j.1748-1716.1976.tb10227.x.
Glucose consumption was measured in the cerebral cortex of rats, anesthetized with 70% N20, under normoxic conditions, as well as in hypoxia (Pao2 about 25 mmHg) and hypercapnia (Paco2 80-85 mmHg). The method used was that Hawkins et al (1974), modified to allow studies of transients in glycolytic rate. Cortical glucose consumption in normoxia was 0.77 mumol-g(-1)-min(-1). It is concluded that whereas glucose consumption in the whole brain of unanesthetized rat may be close to 0.6 mumol-g(-1)-min(-1), that of the cerebral cortex is close to 0.8 mumol-g(-1)-min(-1). During the first 2 min of hypoxia, glucose consumption was increased to twice the normal, and during the fist 2 min of hypercapnia, the corresponding value was less thane third of the normal. After 15 min of hypoxia, the glucose consumption had returned towards control values. In "steady state" hypercapnia, the glycolytic flux was higher than in the inital phase although still below normocapnic values.