Increased ventilatory lung stretch alters the effect of soluble guanylyl cyclase-derived cGMP on endothelial barrier function in isolated mouse lungs

Background Ventilator-induced lung injury (VILI) increases lung endothelial permeability. Lung endothelial nitric oxide (NO) generation contributed to this increased permeability in an intact mouse model of VILI [1]. NO stimulates endothelial soluble guanylyl cyclase (sGC) to produce cGMP. The effect of cGMP on endothelial permeability is controversial [2]. We sought to determine 1) if endothelial cGMP is generated in VILI and 2) if changes in endothelial cGMP modulate VILI-induced endothelial barrier dysfunction.