—(1) The effects of exposure of rats to increased atmospheric concentrations of CO2 on brain metabolism in vivo were studied. (2) After 2·5 min exposure to an atmosphere of 20% CO2, the rate of glucose utilization by brain decreased from 0·61 μmol/min per g to 0·32 μmol/min per g and remained between 0·3 and 0·4 μmol/min per g for 60 min, the longest interval studied. O2 utilization, calculated from the arteriovenous difference of O2 across the brain and blood flow, was 3·5 μmol/min per g in controls and was 4·7 μmol/min per g after 5 min in the 20% CO2 atmosphere. (3) The concentrations of glucose, glucose 6‐phosphate and aspartate were increased during the first 10 min of CO2 exposure whereas the concentrations of other glycolytic intermediates, tricarboxylic acid cycle intermediates and glutamate were decreased. The amount of endogenous substrate which disappeared during the first 10 min was sufficient, if used to supplement glucose as a fuel, to maintain the O2 consumption at, or slightly above, the control level. Glutamate and lactate were quantitatively the most important energy sources. (4) The mechanism whereby‘CO2 decreased the rate of glucose utilization is uncertain. The initial rise in glucose 6‐phosphate and fall in fructose 1,6‐diphosphate concentrations suggested that an inhibition of phosphofructokinase was responsible. However, after 60 min in 20% CO2, the concentrations of both of these metabolites returned to normal while the rate of glucose utilization remained depressed.
|Original language||English (US)|
|Number of pages||6|
|Journal||Journal of neurochemistry|
|State||Published - Nov 1975|
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience