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Tuesday, February 5, 2008

Fetal Alcohol Exposure Alters Cerebrovascular Reactivity to Vasoactive Intestinal Peptide in Adult Sheep
Neonatology 2008;93:45-51


Chronic fetal alcohol exposure impairs neural and vascular development. We have previously shown that fetal alcohol exposure is associated with attenuated hypoxic cerebral vasodilation and reduced neuronal vasoactive intestinal peptide (VIP) expression in fetal sheep.

In the present study, we tested the hypothesis that fetal alcohol exposure alters vascular development, leading to altered cerebral vascular reactivity to VIP in adulthood.

There was no difference in myogenic tone between arterioles exposed prenatally to alcohol (n = 18) and saline controls (n = 17). However, fetal alcohol exposure significantly (p = 0.03) enhanced the dilator responses of adult intracerebral arterioles to VIP [0.1 nM to 1 µM, logEC50: -8.6 ± 0.2 (alcohol) vs. -7.4 ± 0.8 (saline)]. In contrast, there was no difference in dilator responses to H+ (pH 6.8 buffer), to adenosine (10 nM to 0.1 mM), or to CGS21680 (an adenosine A2A receptor agonist, 0.01 nM to 10 µM).

Thus, fetal alcohol exposure alters vasomotor sensitivity to VIP in adult intracerebral arterioles - perhaps a compensatory response to alcohol-induced underdevelopment of neurotransmitter pathways involved in cerebral vascular regulation.

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