Journal of Applied Physiology, Vol 56, Issue 5 1178-1186, Copyright © 1984 by American Physiological Society
Newborn puppy cerebral acid-base regulation in experimental asphyxia and recovery
E. E. Nattie, W. H. Edwards and M. Marin-Padilla
We hypothesized that part of the newborn tolerance of asphyxia involves
strong ion changes that minimize the cerebral acidosis and hasten its
correction in recovery. After exposure of newborn puppies to 15 or 30 min
experimental asphyxia (inhalation of gas with fractional concentration of
CO2 and of O2 in inspired gas = 0.07-0.08 and 0.02-0.03, respectively),
blood lactate increased to 13.2 and 23.4 mmol/l, respectively, brain tissue
lactate increased to 14.4 and 19.7 mmol/kg, and cerebrospinal fluid (CSF)
lactate increased to 7.6 and 14.4 mmol/l. We presume that the tissue
lactate increase reflects increases in brain cell and extracellular fluid
lactate concentration. The lactate increase, a change that will decrease
the strong ion difference (SID), [HCO3-], and pH, was accompanied by
increases in Na+ (plasma, CSF, brain), K+ (plasma, CSF), and osmolality
without change in Cl-. After 60-min recovery, plasma and brain lactate
decreased significantly, but CSF lactate remained unchanged. [H+] recovery
was more complete than that of the strong ions due to
hyperventilation-induced hypocapnia. We conclude that during
asphyxia-induced lactic acidosis, changes in strong ions occur that lessen
the decrease in SID and minimize the acidosis in plasma and CSF. To the
extent that the increase in brain tissue sodium reflects increases in
intra-and extracellular fluid sodium concentration, the decrease in SID
will be less in these compartments as well. In recovery, CSF ionic values
change little; plasma and brain tissue lactate decrease with a similar time
course, and the [H+] is rapidly returned toward normal by hypocapnia even
while the SID is below normal.
