Volume 49, Issue 3 Fall 2025 JVU 493-130 | CO2 Reactivity in Brain Relies on Blood Pressure Regulation as well as Arteriolar Vaso-Reactivity-CO2 Reactivity in Brain Relies on Blood Pressure Regulation as well as Arteriolar Vaso-Reactivity

CO2 Reactivity in Brain Relies on Blood Pressure Regulation as well as Arteriolar Vaso-Reactivity

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This 2025 study in the Journal for Vascular Ultrasound by Chan, Mulder, and Schaafsma investigated the mechanisms underlying carbon dioxide (CO2)-reactivity of the middle cerebral artery blood velocity (MCAv), a key method to assess cerebrovascular physiology and cerebral autoregulation. CO2-reactivity involves measuring changes in cerebral blood flow velocity in response to variations in CO2 levels induced by hyperventilation (lower CO2) or CO2 retention (higher CO2). The research specifically examined whether changes in MCAv during CO2 manipulation are driven by local arteriolar vaso-reactivity, changes in arterial blood pressure (ABP), or both.<br /><br />Fourteen healthy young adults (18-25 years) underwent simultaneous transcranial Doppler ultrasound to measure MCAv and noninvasive continuous ABP monitoring during controlled breathing protocols: rest, hyperventilation (lowering end tidal CO2), normoventilation, and CO2 retention (increasing end tidal CO2). Both signals were analyzed using advanced waveform decomposition to identify first and second systolic peaks (Sys1 and Sys2) and diastolic measurements at 560 ms after systolic upstroke (D560). The study calculated an "apparent resistance" (aR) as the ratio ABP/MCAv to infer changes in cerebrovascular resistance.<br /><br />Key findings include: hyperventilation decreased ETCO2 (~1.9%), reducing MCAv significantly without altering ABP, indicating that MCAv decrease reflects arteriolar vasoconstriction. In contrast, CO2 retention increased ETCO2 (~1.7%) and elevated both MCAv and ABP, while aR remained unchanged, suggesting MCAv increase chiefly results from systemic blood pressure elevation rather than local vasodilation. Heart rate increased with hyperventilation but remained stable during CO2 retention. Waveform analyses indicated differential physiological processes underlying systolic peaks and diastolic components.<br /><br />The authors conclude that CO2-reactivity involves a combination of arteriolar vaso-regulation and systemic ABP regulation, with hyperventilation primarily causing cerebral vasoconstriction and CO2 retention mainly inducing ABP rises via the central nervous system ischemic response. This challenges the traditional view that CO2 retention-induced flow increases solely reflect vasodilation. The study recommends monitoring ABP during CO2-reactivity tests and cautions interpreting cerebral blood flow changes without ABP data. Limitations include the assumption of constant MCA diameter during tests and a predominantly female young adult sample.<br /><br />Overall, this study provides novel insight into the cerebral hemodynamics underlying CO2-reactivity, emphasizing the interplay between cerebral vessel tone and systemic blood pressure in maintaining brain blood flow.

Keywords

CO2-reactivity

middle cerebral artery blood velocity

cerebrovascular physiology

cerebral autoregulation

hyperventilation

arterial blood pressure

transcranial Doppler ultrasound

apparent resistance

cerebral vasoconstriction

systemic blood pressure regulation