Although information on energy metabolism during hypoxemic-ischemic states
is abundant, data on perinatal asphyxia (PA) are limited. As results from h
ypoxia-ischemia cannot be directly extrapolated to PA, a clinical entity ch
aracterized by acidosis, hypoxemia and hypercapnia, we decided to use a rat
model of graded PA during delivery. Cesarean section was performed at the
21st day of gestation and the pups, still in the uterus horns, were asphyxi
ated from 0 to 20 minutes. In this model survival decreases with the length
of asphyxia. Early changes of energy-rich phosphates in brain, heart and k
idney were determined by HPLC. ATP and phosphocreatine gradually decreased
with the length of asphyxia, with highest ATP depletion rate occurring in t
he kidney. ATP: brain 1.39+/-0.71 (0 min) to 0.06 mu M/g wwt (20 min); hear
t 4.73+/-0.34 (0 min) to 1.08+/-0.47 (20 min); kidney 1.62+/-0.11 (0 min) t
o 0.02+/-0.02 (20 min). Phosphocreatine: brain 1.65+/-0.68 (0 min) to 0.5+/
-0.45 mu M/g (20 min); heart 6.98+/-0.38 (0 min) to 6.17+/-1.07 (20 min); k
idney 8.23+/-0.86 (0 min) to 3.76+/-0.54 (20 min). We present data on energ
y derangement in a rat model of PA, closely resembling the clinical situati
on, showing that energy depletion precedes cell damage and death. (C) 2000
Elsevier Science Inc. All rights reserved.