Reproducibility of Brachial Vascular Changes with Alterations in End-Tidal Carbon Dioxide.

The purpose of this study was to examine the reproducibility of the peripheral vascular response to hypercapnia. Healthy college-aged men (n = 7) and women (n = 10) underwent an iso-oxic 10-mm Hg increase in PetCO2 for 12 min. Brachial artery diameter changes were measured using ultrasound imaging. Two tests were completed on day 1 with 15 min of rest between tests. Tests were repeated on day 2. Paired t-tests, Bland-Altman plots and intra-class correlations (ICCs) determined reproducibility. There were no significant differences in peak dilation within day (5.33 ± 3.73% vs. 4.52 ± 2.49%, p = 0.378). The within-day ICC was poor (0.213). Within-day time-to-peak dilation did not significantly differ (660.0 ± 231.8 s vs. 602.7 ± 259.9 s, p = 0.379), and the ICC was fair (0.416, p = 0.113). Between-day peak dilation did not significantly differ (5.24 ± 3.84% vs. 4.71 ± 3.17%, p = 0.123), and the ICC was fair (0.419). Hypercapnia-induced brachial artery dilation is similar within day and between days. The ICC for peak dilation suggests the methodology is not reproducible.

Comparison of brachial dilatory responses to hypercapnia and reactive hyperemia.

Flow-mediated dilation (FMD) relies on reactive hyperemia to stimulate the endothelium to release nitric oxide, causing smooth muscle relaxation. Hypercapnia also produces vasodilation, which is thought to be nitric oxide-independent. The purpose of this study was to compare and contrast the effects of hypercapnia and reactive hyperemia as stimuli for brachial artery dilation. On separate days, twenty-five participants underwent vasodilation studies via reactive hyperemia or hypercapnia (i.e. 10 mmHg increase in end-tidal carbon dioxide [PetCO2)]). During both studies changes in brachial artery diameter were recorded using continuous ultrasound imaging. Heart rate (HR) was measured throughout both tests. Resting HR (63 ± 11 versus 68 ± 14 beats min(-1), p = 0.0027) and baseline brachial artery diameter measurements (4.57 ± 1.51 versus 5.28 ± 1.86 mm, p = 0.022) were significantly different between reactive hyperemia and hypercapnia, respectively. HR at peak dilation (65 ± 11 versus 76 ± 14 beats min(-1), p < 0.0001), peak vessel dilation (8.68 ± 4.50 versus 5.28 ± 1.86%, p = 0.002), and time to peak dilation (90.8 ± 120.1 versus 658.3 ± 226.6 s, p < 0.0001) were also significantly different between reactive hyperemia and hypercapnia. The dynamics by which reactive hyperemia and hypercapnia stimulate vasodilation appear to differ. Hypercapnia produces a smaller and slower vasodilatory effect than reactive hyperemia. Further research is necessary to better understand the mechanisms of vasodilation under hypercapnic conditions.