SYMPATHETIC-NERVE MODULATION OF REGIONAL CEREBRAL BLOOD-FLOW DURING ASPHYXIA IN NEWBORN PIGLETS

Regional cerebral blood flow (rCBF) during asphyxia suggest a reflex vasoconstrictor mechanism active principally in brain cortex. Present studies in newborn piglets investigate sympathetic modulation of the cerebrovasculature both during and after acute asphyxia. Unilateral superior cervical sympathetic ganglionectomy (SCSG) was performed in 13 new born piglets, after which asphyxia was produced by discontinuing ventilation. In 8 animals, blood flow was measured during control and sequentially 1, 2, and 3 min after ventilation was stopped. In 5 piglets with unilateral SCSG, cortical flow decreased in the innervated hemisphere, -34 +/- 14% after 2 min, and -25 +/- 9% at 3 min of asphyxia compared with control (104 +/- 22 ml.min-1.100 g-1; mean +/- SE). In contrast, the sympathetically denervated hemisphere showed -13 +/- 17% at 2 min and + 7 +/- 23% at 3 min, representing 45 +/- 6% and 30 +/- 9% left-right (L-R) flow differences, respectively. Bilateral SCSG (3 piglets) similarly attenuated the cortical CBF vasconstrictor response to asphyxia, +6 +/- 21% at 2 min and -8 +/- 5% at 3 min. Significant innervated-denervated rCBF differences were present during asphyxia in cerebral gray (55% +/- 24), cerebral white (41% +/- 16), caudate (25% +/- 7), hippocampus (36% +/- 12), and choroid plexus (145% +/- 42), indicating sympathetic nerve modulation. Brain stem structures showed increasing rCBF throughout asphyxia and no L-R differences. To evaluate the effect of sympathetic nerves during recovery from asphyxia, 5 additional piglets with unilateral SCSG were studied at control, during asphyxia, and twice after ventilation was resumed: reventilation 1 (34-84 s) and reventilation 2 (174-322 s). L-R differences were abolished in both recovery periods. In the newborn piglet, sympathetic reflex vasoconstriction modulates rCBF during acute asphyxia, but does not attenuate cerebrovascular hyperemia during reventilation.