The effect of steady-state CO2 on regional brain blood flow responses to increases in blood pressure via the cold pressor test

Abstract

The pressure-passive cerebrovasculature is affected by alterations in cerebral perfusion pressure (CPP) and arterial blood gases (e.g., pressure of arterial [Pa]CO₂), where acute changes in either stimulus can influence cerebral blood flow (CBF). The effect of superimposed increases in CPP at different levels of steady-state PaCO₂ on regional CBF regulation is unclear. In 17 healthy participants, we simultaneously recorded continuous heart rate (electrocardiogram), blood pressure (finometer), pressure of end-tidal CO₂ (P_ETCO₂; gas analyzer), and middle (MCA) and posterior (PCA) cerebral artery blood velocity (CBV; transcranial Doppler ultrasound). Three separate CPTs were administered by passive immersion of both feet into 0-1 °C of ice water for 3-min under three randomized and coached steady-state P_ETCO₂ conditions: normocapnia (room air), hypocapnia (-10 Torr; hyperventilation) and hypercapnia (+9 Torr; 5% inspired CO₂;). CBV responses were calculated as the absolute difference (∆) between baseline and mean MCAv and PCAv during the 3-min CPT. Both the ∆MCAv and ∆PCAv responses to the CPT were larger under hypercapnic conditions. The absolute ∆MCAv response was larger than the ∆PCAv during the CPT across all three CO₂ trials. Cerebrovascular CO₂ reactivity (CVR) was larger in the MCA than PCA in both CPT and baseline conditions, but there were no differences in CVR between CPT and baseline conditions. Our data indicate that (a) increases in CO₂ increases the CBV responses to a CPT, (b) the anterior cerebrovasculature is more responsive to a CPT-induced increases in MAP, and (c) although unchanged during a CPT, CVR is larger in the anterior cerebral circulation.

Keywords: Cerebral autoregulation; Cerebral blood flow; Cerebrovascular reactivity; Cold pressor test; Sympathetic nervous system activation.