Miller A L, Shamban A T, Corddry D H, Kiney C A
J Neurochem. 1982 Apr;38(4):916-24. doi: 10.1111/j.1471-4159.1982.tb05330.x.
Brain glucose metabolism was studied in paralyzed, ventilated rats given electroconvulsive shock (ECS) under normocapnic and hypercapnic conditions. Brains were obtained with a freeze-blowing apparatus. Rates of glucose utilization were determined with [2-14C]glucose and [3H]deoxyglucose as tracers. In normocapnic rats, ECS caused a large increase in the rate of glycolysis to 5--6 mumol/g/min. Brain lactate levels increased three- to fourfold. The stimulation of glucose metabolism was reflected in decreased brain glucose 6-phosphate concentration as early as 2--3 s after ECS. There were significant decreases in brain glucose and glycogen levels at 20 and 30 s after ECS. The decreases in endogenous brain glucose accounted for most of the increases in glucose utilization measured isotopically, implying that influx of glucose from blood into brain did not increase greatly over these time periods. Animals made hypercapnic by respiration with 10% CO2 for 2 min prior to ECS were different in their metabolic responses to ECS in several ways. The increases in glycolytic rate and lactate content of brain were half of those found in normocapnic rats. Brain glycogen and glucose concentrations did not change significantly in the hypercapnic rats during seizure activity. Thus, hypercapnia lessened the stimulation of glycolysis caused by ECS, but increased net influx of glucose from blood to brain. The mechanisms of these effects of hypercapnia are uncertain, but it is postulated that the effect on glycolytic activity is due to the acidosis and that the effect on glucose transport is due to an increase in capillary surface area.
