NEWBORN CEREBROVASCULAR RESPONSES AFTER FIRST-TRIMESTER MODERATE MATERNAL ETHANOL EXPOSURE IN SHEEP

Fetal alcohol syndrome is one of the leading causes of mental retardat ion in the United States, but the pathogenesis of the associated brain damage is unknown. We tested the hypothesis that neonatal cerebrovasc ular responses to CO2 and/or hypoxia may be altered by moderate chroni c maternal ethanol exposure early in gestation. We studied 26 newborn lambs (1-4 d old). Their mothers had received daily i.v. infusions of either ethanol (1 g/kg; ethanol concentration = 167 +/- 3 mg/dL; mean +/- SEM) or a similar volume of saline for 3 wk during the first trime ster. In nine lambs, we studied cerebral responses to CO2 (saline, n = 4; ethanol, n = 5) and in 17 lambs, cerebral responses to hypoxia (sa line, n = 7; ethanol, n = 10). Cerebrovascular responses to CO2 were n ot different between the groups. However, the cerebral vasodilatory re sponse to hypoxemia was significantly attenuated in the ethanol lambs, such that cerebral O-2 delivery was not maintained. During severe hyp oxia (arterial Po-2 = 30 mm Hg), cerebral blood flow increased 106 +/- 23% (mean +/- SEM) above baseline in the saline-treated group, but in creased only 32 +/- 15% above baseline in the ethanol-treated group (p < 0.02). Similarly, cerebrovascular resistance in the saline group de creased 52 +/- 6% from baseline, but decreased only 16 +/- 11% in the ethanol group (p < 0.02). We conclude that moderate maternal ethanol i nfusion early in pregnancy attenuates neonatal hypoxic, but not CO2, c erebrovascular responsivity.