Cyclic AMP in cerebrospinal fluid(CSF) of asphyxiated human newborns

We previously found that, in newborn pigs, prolonged asphyxia results in significant decreases in cerebral periarachnoid CSF cAMP during the recovery period. The decreases in cAMP were well correlated with reduced dilator responses to stimuli utilizing cAMP as a second messenger. We hypothesize that prolonged asphyxia can also inhibit cAMP accumulation in human newborn CSF. The normal range of CSF cAMP in newborn babies was determined via CSF of neonates requiring a spinal tap during infection work-up. Babies who had no findings indicative of CNS pathology including negative CSF culture were considered to be the control group ( n= 23). The asphyxiated group consisted of babies with known perinatal asphyxia based on fulfillment of the asphyxia criteria (intrapartum distress, abnormal blood pH, Apgar score, and related clinical findings). These babies required spinal laps as part of a septicemia work-ups, but subsequently were found to have no CNS infection. CSF cAMP was markedly reduced in asphyxiated neonates as compared to nonasphyxiated controls ( 6750+2000 vs. 23800+2200 fmol/ml). We conclude that the CSF cAMP can be used as an adjunct to other tests for confirmation of asphyxia. Further, coupled with the results from asphyxiated newborn pigs, these data suggest inhibition of the cAMP system may compromise cerebrovascular regulation in asphyxiated human newborns.