CHANGES IN CEREBRAL CYCLIC-NUCLEOTIDES AND CEREBRAL BLOOD-FLOW DURINGPROLONGED ASPHYXIA AND RECOVERY IN NEWBORN PIGS

Cerebrovascular reactivity is preserved after acute severe asphyxia/re ventilation in piglets. We hypothesize that prolonged, partial asphyxi a with hypotension causes loss of cerebrovascular reactivity and alter ed cerebral hemodynamics during recovery. We investigated the changes in cerebrospinal fluid cAMP and cGMP, pial arteriolar diameters and fl ow, and cerebral blood flow during 1 h of asphyxia and 1 h of recovery . During asphyxia, blood pressure decreased from 10 +/- 0.7 to 4.7 +/- 0.3 kPa and increased during recovery to 6 +/- 0.7 kPa. cAMP increase d 3-fold by 20 min of asphyxia, returning to baseline at 40 min of asp hyxia. During recovery, cAMP increased 2-fold initially, followed by a decrease to 50% below baseline, cGMP increased after 20 min of asphyx ia, with maximum levels observed at 40 min; reventilation resulted in a transient increase in cGMP. Pial arteriolar diameters increased at t he onset of asphyxia, then decreased toward baseline; during recovery, a similar pattern occurred. Blood flow to the cerebrum (microspheres) decreased during asphyxia and remained very low during recovery. Pial arteriolar flow but not pial arteriolar diameters followed the change s in cortical cerebral blood flow (i.e. virtually no flow during recov ery). During recovery, pial arteriolar reactivity to isoproterenol and histamine decreased significantly. We conclude that 60 min of asphyxi c-hypotensive insult results in alterations of cerebral cAMP metabolis m which may compromise cellular communications during recovery. Prolon ged asphyxia induces ''no-reflow'' during recovery, even when partial pressures of arterial CO2 and O-2 have returned to baseline values, an d blood pressure is within the autoregulatory range.