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1 ion in the respiratory cycle is dependent on S-nitrosohemoglobin.
2 nitric oxide (NO) to cysteinebeta93, forming S-nitrosohemoglobin.
6 terial vs. venous differences in nitrite and S-nitrosohemoglobin are diminished in sepsis and associa
10 groups is a rapidly reversible process, and S-nitrosohemoglobin formation is probably not a primary
12 s accompanied by an allosteric transition in S-nitrosohemoglobin [from the R (oxygenated) to the T (d
13 issue oxygenation and is proportional to RBC S-nitrosohemoglobin (HbSNO) content (but not nitrosylhem
15 sting systemic nitrite consumption), whereas S-nitrosohemoglobin levels are higher in venous vs. arte
17 ologic paradigms contend that nitrite and/or S-nitrosohemoglobin mediate intravascular delivery of ni
19 d relaxations during hypoxia correlated with S-nitrosohemoglobin (SNO-Hb) (R2=0.88) but not iron nitr
24 s results run counter to the hypothesis that S-nitrosohemoglobin (SNO-Hb) serves as an in vivo reserv
25 sial, with separate roles for nitrite () and S-nitrosohemoglobin (SNO-Hb) widely contested given thei
26 itrosation of cysteine beta93 in hemoglobin (S-nitrosohemoglobin (SNO-Hb)) occurs in vivo, and transn
27 , RBC-dependent vasoregulatory function, and S-nitrosohemoglobin (SNO-Hb), through which hemoglobin (
29 the blood is bound to thiols of Hb, forming S-nitrosohemoglobin (SNO-Hb), which releases the NO grou
39 ing nitric oxide bioactivity (in the form of S-nitrosohemoglobin) was markedly diminished 10 hours af
40 te S-nitrosothiol content (reflecting mainly S-nitrosohemoglobin) was significantly higher for blood
42 93 cysteine S-nitrosylated hemoglobin [SNOHb:S-nitrosohemoglobin], which has been shown to induce vas
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