Shear stress-induced restoration of pulmonary microvascular endothelial barrier function following ischemia reperfusion injury requires VEGFR2 signaling

Critical illnesses are frequently complicated by noncardiogenic pulmonary edema. Many such illnesses include periods of reduced blood flow, often accompanied by hemodilution, which together reduce endothelial shear stress. We report that in ischemia-reperfusion injury reduced shear stress contributes to increased permeability of the in situ pulmonary microvascular endothelium and worsens alveolar edema. Restoring shear stress toward normal reduces endothelial permeability and edema formation, an effect that requires the normal mechanoreceptor function of VEGFR2.