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. 2005 Oct 3;102(41):14801–14806. doi: 10.1073/pnas.0506957102

Fig. 4.

Fig. 4.

RBC-NO levels, RBC function, and PAP in patients. (A) Levels of SNO-Hb and Hb[FeNO] in arterial blood of normal human subjects and PAH patients. NO/Hb, mol of NO per mol of Hb (tetramer). *, P < 0.05 vs. normal patients; n = 5-8. (B) SNO content of blood presented as the percentage of total NO bound to Hb. (C) Increased FeNO/SNO signature of PAH. (D) Inverse correlation between RBC-NO levels and PAP. Hb-NO levels (expressed as mol of NO per mol of Hb tetramer) and baseline PAP in 14 patients. (E and F) Vasorelaxation (percent change in initial tension) by RBCs from normal subjects and from PAH patients. (E) Actual tracings of the hypoxia-mediated vasodilator response by RBCs of deendothelialized pulmonary artery [in the presence and absence of the guanylate cyclase inhibitor ODQ [1H(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one] (1 μM)] and intact aortic rings. (F) Mean aortic ring results (±SEM) expressed as the relative area under the time-tension curve (AUC) or as the peak decrease in tension; data are from seven individuals in each group. Hypoxia-mediated vasodilation by RBCs is impaired in PAH. *, P < 0.05 vs. normal subjects.