Lacy M. Alexander

We tested the hypothesis that post‐COVID‐19 adults (PC) would have impaired cutaneous nitric oxide (NO)‐mediated vasodilation compared to controls (CON). We performed a cross‐sectional study including 10 (10 F/0 M, 69 ± 7 years) CON and 7 (2 F/5 M, 66 ± 8 years) PC (223 ± 154 days post‐diagnosis). COVID‐19 symptoms severity (survey) was assessed (0–100 scale for 18 common symptoms). NO‐dependent cutaneous vasodilation was induced by a standardized 42°C local heating protocol and quantified via perfusion of 15 mM NG‐nitro‐L‐arginine methyl ester during the plateau of the heating response (intradermal microdialysis). Red blood cell flux was measured with laser‐Doppler flowmetry. Cutaneous vascular conductance (CVC = flux/mm Hg) was presented as a percentage of maximum (28 mM sodium nitroprusside +43°C). All data are means ± SD. The local heating plateau (CON: 71 ± 23% CVC max vs. PC: 81 ± 16% CVC max , p = 0.77) and NO‐dependent vasodilation (CON: 56 ± 23% vs. PC: 60 ± 22%, p = 0.77) were not different between groups. In the PC group neither time since diagnosis nor peak symptom severity (46 ± 18 AU) correlated with NO‐dependent vasodilation ( r < 0.01, p = 0.99 and r = 0.42, p = 0.35, respectively). In conclusion, middle‐aged and older adults who have had COVID‐19 did not have impaired NO‐dependent cutaneous vasodilation. Additionally, in this cohort of PC, neither time since diagnosis nor symptomology were related to microvascular function.