Objective. To investigate whether or not postasphyctic cerebral hypope
rfusion and decreased cerebral metabolism occur in the perinatally asp
hyxiated neonate, as has been reported in adults and newborn animals.
Methods. Using near-infrared spectroscopy, we monitored changes in oxy
hemoglobin (HbO2), deoxyhemoglobin (HbR), total hemoglobin (HbO2 + HbR
, which represents changes in cerebral blood volume [CBV]), and cytoch
rome oxidase (Cytaa3, which indicates changes in oxidation level of th
is intracerebral mitochondrial enzyme). Thirty-one neonates (gestation
al age >34 weeks), divided into three groups, were monitored between 2
and 12 hours or between 12 and 24 hours of life. Group I consisted of
healthy newborns: N = 8 (2 to 12 hours) and N = 5 (12 to 24 hours). P
atients in group II were moderately asphyxiated newborns but neurologi
cally normal in the first 24 hours of life: N = 6 (2 to 12 hours) and
N = 3 (12 to 24 hours). Group III consisted of severely asphyxiated ne
wborns with an abnormal neurologic behavior within 24 hours after birt
h: N = 5 (2 to 12 hours) and N = 4 (12 to 24 hours). Results. From 2 t
o 12 h, CBV levels in groups I and II were stable. In group III CBV de
creased in all infants. This decrease in CBV was associated with a dro
p in both HbO2 and HbR. Cytaa3 was stable in groups I and II, but show
ed a marked decrease in two of the five infants of group III. There wa
s a positive relationship between CBV and mean arterial blood pressure
in groups II and III. Between 12 and 24 hours, all groups showed stab
le CBV and Cytaa3 patterns. A positive relation existed now between tr
anscutaneous PCO2 and CBV in groups II and III. Conclusions. CBV, HbO2
, HbR, and Cytaa3 decreased in the first 12 hours of life in severely
asphyxiated neonates who subsequently developed neurologic abnormaliti
es. We therefore suggest that posthypoxic-ischemic reperfusion injury
of the brain during early neonatal life occurs in neonates with severe
birth asphyxia.