Normal and Elevated Blood CO2 Increased Anterior Blood Flow Responses During the Cold Pressor Test
The cerebrovasculature is responsive to acute alterations in blood gases (e.g., CO2) and blood pressure. The brain is relatively pressure passive, with acute increases in mean arterial pressure (MAP) driving increases in cerebral blood flow (CBF). The superimposition of dynamic increases in MAP and controlled CO2 perturbations on the regulation of anterior and posterior cerebral circulation is unclear. We aimed to characterize the effects of cold pressor test (CPT) on the anterior and posterior (middle and posterior cerebral arteries; MCA, PCA) with a background of different steady-state CO2 perturbations. Seventeen healthy participants were instrumented with electrocardiogram, finometer, mouthpiece/noseclip, and transcranial Doppler ultrasound (TCD) for measurement of MCA and PCA velocity (MCAv, PCAv). End-tidal CO2 was measured using calibrated CO2 analyzer. In a randomized order, a CPT was administered using 0-2°C water immersion of the lower limbs for 3-min under three coached, normoxic, steady-state end-tidal PCO2 conditions: normocapnia (eupnea), hypocapnia (-10 Torr) and hypercapnia (+8 Torr). The CBV responses were calculated as the absolute difference (∆) between baseline and the mean MCAv and PCAv during the 3-min CPT. The ∆MCAv response was larger in the hypercapnic trial compared to normocapnia and hypocapnia (P<0.05), but there were no differences in the ∆PCAv. The ∆MCAv CPT response was larger than the ∆PCAv during the hypercapnic trial (P<0.001) as well as the normocapnic trial (P=0.017), but there were no differences between ∆MCAv vs. ∆PCAv in the hypocapnic trials. Our data demonstrate that there was differential regional permissive hyperemia when acute increases in MAP and steady-state CO2 are superimposed. Funding Sources: NSERC Discovery, MRU Faculty of Science and Technology.
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