The main novel findings of this study are: (1) in patients with moderate-severe COPD, acute increases in retrograde shear stress and/or reductions in mean shear stress further deteriorate the already impaired endothelial function with attendant endothelial apoptosis, and (2) that supplemental O2 abrogates the oscillatory shear stress-induced increase in CD31+/41b− and improves endothelium-dependent vasodilation for a given stimulus. The gene discussed is PECAM1; the disease is chronic obstructive pulmonary disease.