CO 2 Reactivity in Brain Relies on Blood Pressure Regulation as Well as Arteriolar Vaso-Reactivity

Abstract

Introduction:

Carbon dioxide (CO₂)-reactivity of middle cerebral artery blood velocity (MCAv) is a well-established method to study cerebrovascular physiology. Changing blood CO₂ by hyperventilation or CO₂ retention is an artificial stimulus to the neurovascular coupling of arterioles spread throughout the brain, normally linking blood flow to local neuronal activity.

Methods:

By recording MCAv simultaneously with arterial blood pressure (ABP) in 14 young and healthy volunteers, this study aims to answer the theoretical question of whether changes in MCAv should be ascribed exclusively to cerebral vaso-reactivity, to changes in ABP or to a combination of both. Both signals were analyzed by determining the first (Sys1) and second systolic peak (Sys2) and the diastolic flow velocity 560 ms after upstroke onset (D560).

Results:

Hyperventilation resulted in an average decrease of 1.9% in end tidal CO₂ (ETCO₂) and was accompanied by a significant decrease in MCAv (Sys1 -26, Sys2 -28, and D560 -28 cm/s) whereas ABP parameters remained unaltered (Sys1 +7, Sys2 +5, and D560 -1 mmHg). Carbon dioxide (CO₂) retention resulted in an average increase of 1.7% in ETCO₂ and was accompanied by an increase in MCAv (Sys1 +16, Sys2 +27, and D560 +29 cm/s) as well as in ABP (Sys1 +16, Sys2 +24, and D560 +13 mmHg). The apparent resistance (aR), defined as the ratio of ABP divided by MCAv, increased during hyperventilation (Sys1 +0.5, Sys2 +0.6, and D560 +0.8 mm Hg/cm/s) but remained the same during CO₂ retention (Sys1 +0.02, Sys2 +0.04, and D560 -0.01 mm Hg/cm/s).

Conclusion:

We conclude that in young healthy volunteers, hyperventilation reduces MCAv by arteriolar vasoconstriction whereas CO₂ retention increases MCAv by increasing ABP.