Prolonged Endothelial Dysfunction in Human Arterioles with SARS‐CoV‐2

The vascular endothelium plays a crucial role to regulate vascular tone. Severe acute respiratory syndrome coronavirus‐2 (SARS‐CoV‐2) infection is known to cause vascular endothelial dysfunction. However, the long‐term effects of SARS‐CoV‐2 in resistance vessels remains unknown. This study is designed to test whether endothelium‐dependent vasodilation in human arterioles remains impaired after clearance of SARS‐CoV‐2 virus. Fresh human adipose tissues were obtained as discarded surgical specimens from control subjects (n=15, no SARS‐CoV‐2 exposure, 46.7±4 years) and previously SARS‐CoV‐2 positive subjects (PSPSs: n=8, 35.8±3.8 years). Among PSPSs, the time between positive and negative SARS‐CoV‐2 test results was ≤3 months (n=6) or 8 months (n=2). Isolated arterioles (100‐200 µm) were cannulated under 60 mmHg and examined for diameter changes to acetylcholine (ACh; 10−9 to 10−5 M) and sodium nitroprusside (SNP: 10−9 to 10−4 M) using videomicroscopy. Flow‐mediated dilation (FMD) was recorded at steady‐state during graded increases in intraluminal pressure gradients (5‐100 cm H2O). Dilation to ACh and FMD in arterioles from PSPSs was significantly reduced (ACh max. dilation at 10−5 M: 60±6% vs. 92.8±3.9% in control, n=7‐8, P