• B Wuyam, V Bourlier, J L Pépin, J F Payen, and P Lévy.
• PRETA-TIMC, UMR CNRS 5525, Laboratoire de Physiologie, 38700 La Tronche, France.
• Respir Physiol. 2002 Jan 1; 129 (3): 375-84.

AbstractIn order to investigate the effects of moderate hypoxemia on brain electrical activity and the consequences of an altered cerebro-vascular response to hypoxemia, we recorded changes in electrical activity of the brain in anesthetized rats following unilateral carotid artery ligation (UCAL). In these animals, on the clamped side, cerebral blood flow, whilst normal during normoxia, shows less augmentation during hypoxemia. Six anesthetized (Halothane) Sprague-Dawley rats with UCAL were studied during 20 min periods of baseline (FI(O(2))=30%), hypoxemia (FI(O(2))=9.5%) and recovery (FI(O(2))=30%): mean arterial pressure of oxygen (PA(O(2))) achieved was 177.0, 37.6 and 160.1 mmHg, respectively. A significant decrease in the frequencies of the ECoG was observed bilaterally during hypoxemia: centroid frequency (fc)=3.37+/-0.14 and 2.85+/-0.13 Hz on the intact and clamped hemisphere respectively during hypoxemia versus fc=4.09+/-0.20 Hz (mean+/-S.E.M.) during baseline, which was not reversed during recovery (3.27+/-0.11 Hz) (ANOVA, P<0.01). The total power of the signal (Pw) was unaffected on the intact hemisphere but diminished on the clamped side during hypoxemia. Our results show that a significant slowing of ECoG is observed during hypoxemia of moderate intensity (40 mmHg) even when cerebro-vascular response to hypoxemia is preserved and that total power of the ECoG signal is severely diminished when the cerebro-vascular response to hypoxemia is impaired.

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