Cerebral blood flow responses to changes in oxygen and carbon dioxide in humans

This study characterized cerebral blood flow (CBF) responses in the middle cerebral artery to P-CO2 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 cerebral blood velocity was measured using a transcranial Doppler ultrasound. Ventilation (VE), end-tidal P-CO2 (P-ETCO2), and mean arterial blood pressure (MAP) data were also collected. CBF increased with rising P-ETCO2 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-ETCO2 increased 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 CO2 during hypoxic and hyperoxic rebreathing) was likely not due to P-CO2 or perfusion pressure, since P-ETCO2 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.