Brachial artery responses to acute hypercapnia: The roles of shear stress and adrenergic tone, 2022, Jay M. J. R. Carr et al

"Upper limb tissues are, on average, almost as sensitive to CO2 as the brain, but are vasculature supplying them is typically sympathetically constrained".


Abstract
New Findings

• What is the central question of this study?

• We assessed the contributions of shear stress to brachial artery vasodilation during hypercapnia, using a within-individual bilateral experimental design, with increases in shear stress in one artery prevented via manual arterial compression. We repeated this design with and without an α₁-adrenergic receptor blockade, in a placebo-controlled, double-blind, randomized and counterbalanced study, in order to assess the contribution of shear stress during the absence of sympathetic tone.

• What is the main finding and its importance?

• In healthy young adults, shear-mediated vasodilation does not occur in the brachial artery during hypercapnia, as elevated α₁-adrenergic activity typically maintains vascular tone and offsets distal vasodilation controlling flow.

Abstract
We aimed to assess the shear stress-dependency of brachial artery (BA) responses to hypercapnia, and the α₁-adrenergic-restraint of these responses. We hypothesized that elevated shear stress during hypercapnia would cause BA vasodilation, but where shear stress was prohibited (via arterial compression) the BA would not vasodilate (study 1); and, in the absence of α₁-adrenergic activity, blood flow, shear stress and BA vasodilation would increase (study 2).

In study one, 14 healthy adults (7/7 male/female, 27 ± 4 years) underwent bilateral BA Duplex ultrasound during hypercapnia [partial pressure of end-tidal carbon dioxide, +10.2 ± 0.3 mmHg above baseline, 12 minutes] via dynamic end-tidal forcing, and shear stress was reduced in one BA using manual compression (compression vs. control arm).

Neither diameter nor blood flow were different between baseline and the last minute of hypercapnia (P = 0.423, P = 0.363, respectively) in either arm. The change values from baseline to the last minute, in diameter (%; P = 0.201), flow (mL/min; P = 0.234), and conductance (mL/min/mmHg; P = 0.503) were not different between arms.

In study two, 12 healthy adults (9/3 male/female, 26 ± 4 years) underwent the same design with and without α1 adrenergic receptor blockade (Prazosin; 0.05 mg/kg) in a placebo-controlled, double-blind, and randomized design. BA flow, conductance and shear rate increased during hypercapnia in the Prazosin control arm (interaction, P < 0.001), but in neither arm during placebo.

Even in the absence of α₁-adrenergic restraint, downstream vasodilation in the microvasculature during hypercapnia is insufficient to cause shear-mediated vasodilation in the brachial artery.

https://physoc.onlinelibrary.wiley.com/doi/10.1113/EP090690