Rjt. Corbett et al., EFFECT OF HYPOXIA ON GLUCOSE-MODULATED CEREBRAL LACTIC-ACIDOSIS, AGONAL GLYCOLYTIC RATES, AND ENERGY-UTILIZATION, Pediatric research, 39(3), 1996, pp. 477-486
Newborn and 1-mo-old swine were exposed to identical durations (18 min
) and degrees of hypoxia (O-2 content = 4 mL/dL), to examine the effec
ts of hypoxia on cerebral energy metabolism and intracellular pH (pH(i
)) in vivo, using P-31 and H-1 nuclear magnetic resonance spectroscopy
. Hypoxia produced the same extent of reductions in phosphocreatine (P
Cr) (63 +/- 28% and 65 +/- 10%, newborns and 1-mo-olds, respectively)
and pH(i) (6.93 +/- 0.06 and 6.89 +/- 0.06, respectively) for either a
ge group. The magnitude of changes in PCr, lactate, and pH(i) was larg
er for subgroups of data collected when cardiovascular instability was
present, suggesting that hypotension and possibly reduced cerebral pe
rfusion contributed to cerebral energy failure and lactic-acidosis for
either age group. There were no correlations between the blood plasma
glucose concentration at 18 min of hypoxia and the extent of change i
n PCr, lactate, or pH(i) for either age group. During a subsequent per
iod of complete ischemia induced via cardiac arrest after 20 min hypox
ia, the decline in PCr and nucleoside triphosphate (NTP), and increase
in lactate followed similar rates compared with previously studied ag
e-matched animals that were normoxic before ischemia. The rate constan
ts for the change in PCr, NTP, and lactate during ischemia showed no c
orrelation with the blood plasma glucose concentration measured immedi
ately before cardiac arrest. These results suggest that cerebral glyco
lytic rates and energy utilization during ischemia are unaffected by a
preceding interval of hypoxia and that hyperglycemia does not delay c
erebral energy failure during hypoxia or combined hypoxic-ischemia.