Fig. 5.

Role of iNOS in septic PMVEC permeability barrier dysfunction, death and apoptosis 4 h following CLP-sepsis in mice in vivo. As compared to septic wild-type (WT) mice, iNOS deficiency (Nos2 ^−/−) was associated with complete attenuation of septic increases in (a) pulmonary microvascular EB-albumin leak, (b) PMVEC death, and (c) PMVEC apoptosis (FLIVO+, TUNEL+). n = 3–4 (Sham) and n = 3–6 (CLP). * p < 0.05 and ** p<0.01, CLP vs. respective sham group; # p < 0.05, Nos2 ^−/− vs. wild-type CLP