Ethanol attenuates lactate production in hypoxic postnatal day 4 rat cerebella

Ethanol consumption during pregnancy may lead to a low oxygen supply to the brain of the developing fetus. Such a reduction in the oxygen supply will result in changes in intra- and extracellular lactate production, which sub sequently may lead to cytoplasmic acidosis, changes in cerebral metabolism, and eventually, cell death. We used a novel application of gas chromatogra phy to measure lactate changes, on a global level, in the cerebellar tissue of postnatal day (PD) 4 and PD 10 rat pups following in vitro exposure of either hypoxia or hypoxia plus ethanol (hypoxia/ethanol). The results showe d hypoxia-induced increases in lactate concentrations as a function of trea tment time in both PD 4 and PD 10 cerebellar tissue. However, there was a d ifferential response to the additional ethanol treatment between the two ag e groups assessed, with an attenuation of the time-dependent increase of la ctate production following hypoxia treatment in PD 4 cerebellar tissue. The results also indicated that PD 4 cerebellar tissue had increased oxygen ut ilization when compared with PD 10 tissue exposed to the same conditions. T he ethanol-induced reduction in lactate is hypothesized as being due to lim itations in glucose transport and utilization under ethanol/hypoxia exposur e. It is believed that such limitations in cellular function may initiate a sequence of events that produce at least some of the cerebellar neuronal l oss reported in the fetal alcohol literature. (C) 1999 Elsevier Science Inc . All rights reserved.