Differences in Hypercapnia‐Induced Cerebral Vasodilation Between Young, Black Men and Women

Abstract

In the U.S., stroke prevalence and age-adjusted mortality are greater in the black population than all other racial/ethnic groups. Further, black women (BW) exhibit an ~15% lower age-adjusted stroke mortality than black men (BM), suggesting either cerebrovascular protection in BW or cerebrovascular impairment in BM. While the mechanisms underlying the increased burden of stroke in black individuals remain incompletely understood, vascular dysfunction likely contributes to these negative health outcomes. Our group and others have previously demonstrated impaired vasodilation in the brachial artery, cutaneous microvasculature, and cerebral vasculature in black versus white men and women. However, investigations into gender differences in young, black individuals' cerebral vasodilatory responsiveness remain lacking. Therefore, this study tested the hypothesis that BW and BM exhibit divergent cerebral vasodilatory responses to a rebreathing-induced hypercapnic stimulus. To test this hypothesis, 11 BW and 15 BM (mean ± SD; age: 22 ± 4 vs. 23 ± 3) participated in this study. Each participant was instrumented for the continuous measurement of end-tidal carbon dioxide concentration (PETCO2; capnograph), beat-to-beat mean arterial pressure (MAP; finger photoplethysmography), and middle cerebral artery velocity (MCAv; transcranial Doppler ultrasound) at baseline and during rebreathing induced-hypercapnia. Absolute cerebral vascular conductance index (CVCi = MCAv/MAP) and percent change CVCi (ΔCVCi = [CVCiΔPETCO2 – CVCiBL]/CVCiBL • 100) were calculated at baseline and a ΔPETCO2 of 3, 6, 9, and 12 mmHg (only 8 BW were analyzed at 12 mmHg due to some individuals not reaching this stage). No differences in MAP were observed between BW and BM at baseline or any ΔPETCO2 (BL: 91 ± 9 vs. 89 ± 7 mmHg; Δ3: 88 ± 11 vs. 88 ± 9 mmHg; Δ6: 93 ± 8 vs. 89 ± 8 mmHg; Δ9: 94 ± 8 vs. 90 ± 9 mmHg; Δ12: 95 ± 10 vs. 91 ± 9 mmHg; interaction P = 0.11). At baseline, BW had a greater absolute CVCi than BM (0.80 ± 0.10 vs. 0.68 ± 0.13 cm/s/mmHg; P = 0.04). This pattern was also observed at each ΔPETCO2 stage (Δ3: 0.91 ± 0.11 vs. 0.67 ± 0.13 cm/s/mmHg; Δ6: 0.98 ± 0.10 vs. 0.71 ± 0.12 cm/s/mmHg; Δ9: 1.04 ± 0.09 vs. 0.78 ± 0.13 cm/s/mmHg; Δ12: 1.11 ± 0.11 vs. 0.80 ± 0.16 cm/s/mmHg; all P < 0.001). Despite the baseline differences between groups, BW still exhibited a greater ΔCVCi at each stage of ΔPETCO2 than BM (Δ3: 12.9 ± 5.3 vs. 0.1 ± 9.4%; Δ6: 23.0 ± 6.8 vs. 5.5 ± 10.2%; Δ9: 29.9 ± 12.9 vs. 16.0 ± 11.2%; Δ12: 40.7 ± 16.8 vs. 19.0 ± 12.3%; all P < 0.05). These data suggest that young, BW exhibit greater cerebrovascular responsiveness to a hypercapnic stimulus relative to young, BM, which may partially explain the lower age-adjusted stroke mortality in BW. However, the mechanisms responsible for these observed differences remain undetermined and should be the subject of future research.