Fetal cerebral blood flow, electrocorticographic activity, and oxygenation: responses to acute hypoxia

Arterial blood gases are critical in regulation of cerebral blood flow (CBF) and cerebral metabolic rate for O(2) (CMRO(2)). However, the relation of these variables to cortical tissue (t ), and electrocorticographic (ECoG) activity (high voltage low frequency, HVLF, versus low voltage high frequenc...

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Published inThe Journal of physiology Vol. 587; no. Pt 9; pp. 2033 - 2047
Main Authors Lee, Stephen J, Hatran, Douglas P, Tomimatsu, Takuji, Peña, Jorge Pereyra, McAuley, Grant, Longo, Lawrence D
Format Journal Article
LanguageEnglish
Published England 01.05.2009
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Summary:Arterial blood gases are critical in regulation of cerebral blood flow (CBF) and cerebral metabolic rate for O(2) (CMRO(2)). However, the relation of these variables to cortical tissue (t ), and electrocorticographic (ECoG) activity (high voltage low frequency, HVLF, versus low voltage high frequency, LVHF), are not well defined. In the fetus, we tested the hypothesis that ECoG pattern is associated closely with cerebral oxygenation. In fetal sheep (n = 8) with laser Doppler flowmeter, fluorescent O(2) probe and ECoG electrodes, we measured laser Doppler CBF (LD-CBF), tP(O2), ECoG and spectral edge frequency-90 (SEF(90)) in response to 40 min isocapnic hypoxia. In the normoxic fetus, LD-CBF and CMRO(2) correlated highly with ECoG state. With a shift from HVLF to LVHF, tP(O2) decreased followed by increased LD-CBF (18%) and CMRO(2) (13%). With acute hypoxia (P(aO2)= 12 +/- 1 Torr), tp(O2) decreased toapproximately 3 Torr, LD-CBF increased 48 +/- 10%, ECoG shifted to chiefly the HVLF state, SEF(90) decreased approximately 15%, and CMRO(2) decreased approximately 20% (P < 0.05 for each). For the normoxic fetus, CBF was closely related to ECoG state, but this association was less evident during acute hypoxia. We speculate that, in the otherwise stressed fetus, acute hypoxia may further compromise cerebral oxygenation.
ISSN:0022-3751
1469-7793
DOI:10.1113/jphysiol.2008.166983