Journal of Applied Physiology, Vol 78, Issue 6 2272-2278, Copyright © 1995 by American Physiological Society
Effects of hypercapnia on ECoG and oxidative metabolism in neonatal dog brain
H. Yoshioka, H. Miyake, D. S. Smith, B. Chance, T. Sawada and S. Nioka
Department of Biochemistry and Biophysics, University of Pennsylvania, Philadelphia 19104-6089, USA.
The effects of hypercapnia on cerebral electrical activity and
mitochondrial oxidative phosphorylation were studied in the anesthetized
neonatal dog by using the electrocorticogram (ECoG) and 31P-magnetic
resonance spectroscopy. Three levels of hypercapnia with arterial PCO2
values of approximately 70, 100, and 140 Torr reduced the intracellular pH
of the brain from 7.11 to 6.99, 6.87, and 6.76, respectively. These levels
of hypercapnia also reduced ADP concentration ([ADP]) from 21.5 to 18.1,
14.8, and 12.9 microM as well as the average ECoG power output by 20, 30,
and 40%. A Michaelis-Menten relationship for the mitochondrial respiratory
enzymes was fitted with [ADP] and the change in the average ECoG. The
result suggests that mitochondrial respiration is regulated by [ADP] and
that the in vivo Michaelis-Menten constant for ADP was 21 microM, a value
close to the in vitro value. The mitochondrial maximal reaction velocity
was reduced by only 10% during hypercapnia and showed no relationship with
the degree of acidosis, suggesting that mitochondrial respiratory enzymes
are not responsible for the inhibition of the brain electrical activity.
