Cerebral blood flow responses to changes in oxygen and carbon dioxide in humans Andrea Vovk, David A. Cunningham, John M. Kowalchuk, Donald H. Paterson, and James Duffin Abstract: This study characterized cerebral blood flow (CBF) responses in the middle cerebral artery to P CO 2 ranging from 30 to 60 mmHg (1 mmHg = 133.322 Pa) during hypoxia (50 mmHg) and hyperoxia (200 mmHg). Eight subjects (25 ± 3 years) underwent modified Read rebreathing tests in a background of constant hypoxia or hyperoxia. Mean ce- rebral blood velocity was measured using a transcranial Doppler ultrasound. Ventilation (VE), end-tidal P CO 2 (P ETCO 2 ), and mean arterial blood pressure (MAP) data were also collected. CBF increased with rising P ETCO 2 at two rates, 1.63 ± 0.21 and 2.75 ± 0.27 cm·s –1 ·mmHg –1 (p < 0.05) during hypoxic and 1.69 ± 0.17 and 2.80 ± 0.14 cm·s –1 ·mmHg –1 (p < 0.05) during hyperoxic rebreathing. VE also increased at two rates (5.08 ± 0.67 and 10.89 ± 2.55 L·min –1 ·mmHg –1 and 3.31 ± 0.50 and 7.86 ± 1.43 L·min –1 ·mmHg –1 ) during hypoxic and hyperoxic rebreathing. MAP and P ETCO 2 in- creased linearly during both hypoxic and hyperoxic rebreathing. The breakpoint separating the two-component rise in CBF (42.92 ± 1.29 and 49.00 ± 1.56 mmHg CO 2 during hypoxic and hyperoxic rebreathing) was likely not due to P CO 2 or perfusion pressure, since P ETCO 2 and MAP increased linearly, but it may be related to VE, since both CBF and VE exhibited similar responses, suggesting that the two responses may be regulated by a common neural linkage. Key words: brain blood flow, middle cerebral artery, ventilation, mean arterial blood pressure. Résumé : La présente étude a caractérisé les réponses du débit sanguin cérébral (DSC) à une P CO 2 , comprise entre 30 et 60 mmHg (1 mmHg = 133.322 Pa), dans l’artère cérébrale moyenne (ACM), en conditions d’hypoxie (50 mmHg) et d’hyperoxie (200 mmHg). Huit sujets (25 ± 3 ans) ont été soumis à des tests de ré-inhalation de Read modifiés, dans un contexte d’hypoxie ou d’hyperoxie constante. Le DSC moyen a été mesuré par Doppler transcrânien. La ventilation (VE), la P ETCO 2 et la pression artérielle moyenne (PAM) ont aussi été mesurées. Le DSC a augmenté avec l’élévation de la P ETCO 2 à deux valeurs, 1,63 ± 0,21 et 2,75 ± 0,27 cm·s –1 ·mmHg –1 (p < 0,05) durant la ré-inhalation hypoxique et 1,69 ± 0,17 et 2,80 ± 0,14 cm·s –1 ·mmHg –1 (p < 0,05) durant la ré-inhalation hyperoxique. La VE a aussi augmenté (5,08 ± 0,67 et 10,89 ± 2,55 L·min –1 ·mmHg –1 ; 3,31 ± 0,50 et 7,86 ± 1,43 L·min –1 ·mmHg –1 ) durant la ré-inhalation hypoxique et la ré-inhalation hyperoxique. La PAM et la P ETCO 2 ont augmenté linéairement durant les deux modes de ré-inhalation. Le seuil de rupture séparant l’élévation à deux composantes du DSC (42,92 ± 1,29 et 49,00 ± 1.56 mmHg CO 2 durant la ré-inhalation hypoxique et hyperoxique) n’a probablement pas été causé par la P CO 2 ou la pression de perfusion, puisque la P ETCO 2 et la PAM ont augmenté linéairement; toutefois, il pourrait être associé à la VE étant donné que le DSC et la VE ont eu des réponses similaires, ce qui conduit à penser que les deux réponses pourraient être régulées par une liaison neurale commune. Mots clés : débit sanguin cérébral, artère cérébrale moyenne, ventilation, pression artérielle moyenne. [Traduit par la Rédaction] Vovk et al. 827 Introduction Cerebral blood flow (CBF) varies with O 2 and CO 2 such that it increases during hypercapnia and hypoxia (Aaslid et al. 1982; Hauge et al. 1980; Bicher 1974; Heistad and Abboud 1980; Leniger-Follert et al. 1975), decreases during hypocapnia (Bicher 1974; Leniger-Follert et al. 1975), and either decreases or is unchanged during hyperoxia (Bergo and Tyssebotn 1995; Bew et al. 1994). Furthermore, there is an interaction between the effects of O 2 and CO 2 ; the CBF response to CO 2 is enhanced if O 2 is less than 10% but addi- tive otherwise (Quint et al. 1980; Fortune et al. 1992), and hyperoxia only decreases CBF during hypercapnia (Ellingsen et al. 1987). Studies using steady-state methods to measure CBF reac- tivity to increasing CO 2 are disadvantaged for two reasons. First, end-tidal P CO 2 (P ETCO 2 ) is less than brain tissue P CO 2 (P BCO 2 ), and as the CO 2 perturbation increases, the gradient Can. J. Physiol. Pharmacol. 80: 819–827 (2002) DOI: 10.1139/Y02-105 © 2002 NRC Canada 819 Received 7 December 2001. Published on the NRC Research Press Web site at http://cjpp.nrc.ca on 19 August 2002. A. Vovk and D.H. Paterson. 1 School of Kinesiology, University of Western Ontario, London, ON N6A 5C1, Canada. D.A. Cunningham and J.M. Kowalchuk. School of Kinesiology and Department of Physiology, University of Western Ontario, London, ON N6A 5C1, Canada. J. Duffin. Departments of Physiology and Anaesthesia, University of Toronto, Toronto, ON M5S 1A8, Canada. 1 Corresponding author (e-mail: dpaterso@uwo.ca).