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1 ized in 4 steps from methyl vinyl ketone and sodium nitrite.
2 ity phase 1 dose-escalation trial of topical sodium nitrite.
3 s was completely inhibited by a low level of sodium nitrite.
4 rite and reacts with hemoglobin similarly to sodium nitrite.
5 s highly susceptible to killing by acidified sodium nitrite.
6  randomized to receive intracoronary (10 mL) sodium nitrite (1.8 mumol) or NaCl (placebo) before ball
7                                           IV sodium nitrite (10 mug/kg/min) for 1 hour.
8            Our results indicate that topical sodium nitrite 2% cream is suitable for additional clini
9    Active treatment was divided as low dose (sodium nitrite, 3%, with citric acid, 4.5%, creams appli
10 of reperfusion in the absence or presence of sodium nitrite (30 nmol) administered topically 1 min be
11                Intravenous administration of sodium nitrite (48 nmol) 5 minutes before infusion of mu
12  system by mixing a solution of KY jelly and sodium nitrite (5% weight/volume), with a solution of KY
13 %, creams applied twice daily), middle dose (sodium nitrite, 6%, with citric acid, 9%, creams applied
14 cebo applied in the morning), and high dose (sodium nitrite, 6%, with citric acid, 9%, creams applied
15                                       Use of sodium nitrite, 6%, with citric acid, 9%, twice daily is
16       Systemic intravenous administration of sodium nitrite (8.7 mumol/min) dilated the radial artery
17                                Intrabrachial sodium nitrite (8.7 mumol/min) increased radial artery d
18 cise before and after treatment with inhaled sodium nitrite (90 mg) or placebo.
19                                      Topical sodium nitrite, a known nitric oxide donor, enhances blo
20           In this study, the effects of 1 mM sodium nitrite, a reactive nitrogen species (RNS) genera
21 rein, is investigated the effects of topical sodium nitrite administration in a rat model of renal is
22  were given inhaled NO gas (20 ppm), inhaled sodium nitrite aerosol (0.87 mol/L), or an intravascular
23                            Administration of sodium nitrite after severe subarachnoid hemorrhage diff
24 th metabolic syndrome after 12 weeks of oral sodium nitrite and nitrate treatment (IND#115926) displa
25 n spectra of wastewater solutions containing sodium nitrite and nitrate were measured in the concentr
26 es, followed by their alpha-nitrosation with sodium nitrite and subsequent base mediated intramolecul
27 ch as potassium ferricyanide, hydroxylamine, sodium nitrite, and 4-dimethylaminophenol (DMAP), added
28 nts, and quantification of hydroxylamine and sodium nitrite as end reaction products.
29 alide source and tert-butyl nitrite (TBN) or sodium nitrite as the diazotization reagent.
30  of most strains exposed to either acidified sodium nitrite (ASN) or hydrogen peroxide (H(2)O(2)) was
31 bacterium tuberculosis isolates to acidified sodium nitrite (ASN) were compared.
32 ro than other clinical isolates to acidified sodium nitrite (ASN), a generator of reactive nitrogen a
33 at higher rates in the presence of acidified sodium nitrite (ASN), a model system used to generate ni
34 isolate 97A 2472) was resistant to acidified sodium nitrite (ASN).
35 ow in a time-dependent manner, with low-dose sodium nitrite being most effective.
36           To test this, we delivered inhaled sodium nitrite by aerosol to newborn lambs with hypoxic
37 as treated with a different concentration of sodium nitrite cream (cohort 1: 0.5%, cohort 2: 1.0%, co
38                 Increasing concentrations of sodium nitrite cream were applied twice weekly for 4 wee
39  scavenger carboxy PTIO completely abolished sodium nitrite-dependent ischemic tissue blood flow and
40             Nevertheless, higher addition of sodium nitrite elevated the residual nitrite content, re
41                            Administration of sodium nitrite had little effect in normoxia, but produc
42 lly converted to 4 in 45% yield by employing sodium nitrite in aqueous tartaric acid at 0-5 degrees C
43 olerability, and pharmacokinetics of topical sodium nitrite in patients with sickle cell disease and
44                                        Acute sodium nitrite infusion favorably attenuates hemodynamic
45 ency ratio was measured before and during IV sodium nitrite infusion.
46                          Here we report that sodium nitrite (intraperitoneal, inhaled, or oral) limit
47 ntervention, including inhaled nitric oxide, sodium nitrite, L-arginine, phosphodiesterase-5 inhibito
48 ble myocardial ischemia, saline and low-dose sodium nitrite (NaNO(2)) (1.5 mumol/min for 20 min) were
49 or the nitric oxide (NO)-generator acidified sodium nitrite (NaNO(2)) during aerobic growth.
50 only marginally dilating resistance vessels, sodium nitrite (NaNO2) infusion would increase cardiac o
51 ham and acquire new knowledge on the role of sodium nitrite on the formation of its aroma.
52 ects of local and systemic administration of sodium nitrite on the radial artery (a muscular conduit
53 efore and 15 min after treatment with either sodium nitrite or matching placebo.
54 ous therapeutic doses (8.25-3,300 mug/kg) of sodium nitrite or PBS were administered.
55 A subset of HFpEF subjects (n = 52) received sodium nitrite or placebo therapy in a 1:1 double-blind,
56                                              Sodium nitrite (or saline as control) was then infused i
57 ings demonstrate that topically administered sodium nitrite protects the rat kidney against I/R injur
58              Acute administration of inhaled sodium nitrite reduces biventricular filling pressures a
59                                              Sodium nitrite significantly restored ischemic hind-limb
60 h hydrogen peroxide (H(2)O(2)) and acidified sodium nitrite than were the other strains tested.
61 ceived the highest concentrations of topical sodium nitrite (the 1.8% and 2% cream).
62                                              Sodium nitrite therapy also increased ischemic tissue ni
63                          We examined whether sodium nitrite therapy altered ischemic revascularizatio
64    Here, we test the hypothesis that chronic sodium nitrite therapy can selectively augment angiogeni
65                                              Sodium nitrite therapy completely restored ischemic hind
66                        We have reported that sodium nitrite therapy exerts cytoprotective effects aga
67          These data demonstrate that chronic sodium nitrite therapy is a recently discovered therapeu
68                   Remarkably, the effects of sodium nitrite therapy were evident within 3 days of the
69 strating the potency and efficacy of chronic sodium nitrite therapy.
70                     Here we show that adding sodium nitrite to cobinamide yields a stable derivative
71 lm with or without the addition of 10 microM sodium nitrite to the perfusion medium.
72           Meat samples were pre-treated with sodium nitrite to transform oxymyoglobin and deoxymyoglo
73 o a cerebral nitric oxide donor (intravenous sodium nitrite) to explore whether this correlates with
74                       Application of topical sodium nitrite was associated with a significant increas
75 n energy for the reaction of morpholine with sodium nitrite was found as 101 kJ/mol.
76  analysis showed that systemic absorption of sodium nitrite was very low.
77                                 Solutions of sodium nitrite were administered in the setting of hepat
78                                  Intravenous sodium nitrite, which is converted to nitric oxide in vi

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