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1 pretreatment (e.g., increases in circulating free hemoglobin).
2 attributed to scavenging by circulating cell-free hemoglobin.
3 ith severe sepsis and detectable plasma cell-free hemoglobin.
4 as not associated with an increase in plasma-free hemoglobin.
5 ompared with the P(50) of 13.1 Torr for cell-free hemoglobin.
6 hemodynamic reactions or increases in plasma free hemoglobin.
7 -L-arginine (L-NMMA, 10 micromol/L; n=10) or free hemoglobin (1 micromol/L; n=8), preload-induced inc
8 H levels closely correlated with plasma cell-free hemoglobin, accelerated NO consumption by plasma, a
9    Plasma levels of arginine, arginase, cell-free hemoglobin, ADMA, symmetric-dimethylarginine (SDMA)
10 hemolysis was assessed from plasma levels of free hemoglobin and arginase-1.
11 riking nonlinear relationship between plasma free hemoglobin and both TR jet velocity and FMD.
12              Haptoglobin (Hp) scavenges cell-free hemoglobin and correlates with the prognosis of hum
13 ading to intravascular hemolysis, release of free hemoglobin and heme, and increased adhesion of bloo
14 ays in mice) increases plasma levels of cell-free hemoglobin and heme.
15 ed with chronic hemolysis with elevated cell-free hemoglobin and heme.
16 rocytes to prevent the toxic effects of cell-free hemoglobin and heme.
17 ging results with new preparations of stroma-free hemoglobin and hypertonic salt solutions with collo
18 nd resolution of inflammation and removal of free hemoglobin and is highly expressed in myeloid cells
19                   This circulation increased free hemoglobin and LDL- levels compared with non-circul
20 from a caged NO compound, we found that both free hemoglobin and microparticles react with NO about 1
21                                  Plasma cell-free hemoglobin and nitric oxide (NO) consumption capabi
22 inical studies of solutions of modified cell-free hemoglobin and of perfluorocarbon emulsions have de
23 t be measured due to interferences of stroma-free hemoglobin and PHP.
24 MD were most strongly associated with plasma free hemoglobin and transfusion status (transfusions bei
25        Mortality in Ringer's acetate, stroma-free hemoglobin, and 10% pentastarch treated animals was
26 % for whole blood and 4% PHP, 86% for stroma-free hemoglobin, and 33% for 8% PHP.
27                            Serum creatinine, free hemoglobin, and ferritin were measured preoperative
28 tic iron, total iron, transferrin, ferritin, free hemoglobin, and hepcidin with 60-day mortality.
29  elevated concentrations of circulating cell-free hemoglobin are independently associated with an inc
30                      Our data do not support free hemoglobin as a significant contributor to toxicity
31 rts these color values to a concentration of free hemoglobin, based on a built-in calibration curve,
32 logy for improved transport containers, cell-free hemoglobin-based oxygen carriers, freeze-dried bloo
33 deleterious vasoconstrictive effects of cell-free, hemoglobin-based blood substitutes have been appre
34 hindering the clinical development of a cell-free, hemoglobin-based oxygen carrier (HBOC) is systemic
35                          The ability of cell-free hemoglobin blood substitutes to affect vascular ton
36  bioavailability due to the presence of cell-free hemoglobin (CFH) increases vascular tone in severe
37 multiple organ injury, plasma iron, and cell-free hemoglobin (CFH) levels depending on the age of sto
38     Hemolysis and consequent release of cell-free hemoglobin (CFHb) impair vascular nitric oxide (NO)
39 O consumption is correlated with plasma cell-free hemoglobin concentration.
40 rvivors had significantly higher plasma cell-free hemoglobin concentrations (median 20mg/dL, interqua
41  measurements were performed and plasma cell-free hemoglobin concentrations were measured.
42 ntial confounders, patients with higher cell-free hemoglobin concentrations were significantly more l
43                                  Next, while free hemoglobin continued to be infused, the lambs were
44                                       Plasma-free hemoglobin did not change.
45 cetate, 10% pentastarch, or 4 g/dL of stroma-free hemoglobin, followed by aortic repair and transfusi
46                   Haptoglobin (Hp) scavenges free hemoglobin following malaria-induced hemolysis.
47 obin acts as a primary defense by binding to free hemoglobin, forming a haptoglobin-hemoglobin (HpHb)
48                                              Free hemoglobin from ongoing hemolysis scavenges nitric
49        This study evaluates the influence of free hemoglobin generation during CPB and the capacity t
50                                              Free hemoglobin (Hb) and red blood cells augment hypoxic
51                                              Free hemoglobin (Hb) augments hypoxic pulmonary vasocons
52                Haptoglobin binds and removes free hemoglobin (Hb) from the circulation.
53 ptoglobin-related protein (Hpr), which binds free hemoglobin (Hb) in blood and facilitates the uptake
54           Hemolysis and accumulation of cell-free hemoglobin (Hb) in the circulation or in confined t
55                                         Cell-free hemoglobin (Hb) is being developed as an erythrocyt
56                    Systemic exposure to cell-free hemoglobin (Hb) or its breakdown products after hem
57                    It has been reported that free hemoglobin (Hb) reacts with NO at an extremely high
58      Although mature HP is known to scavenge free hemoglobin (Hb) to inhibit its oxidative activity,
59                                              Free hemoglobin (Hb) within the subarachnoid space has b
60 tic lesions, intraplaque hemorrhage releases free hemoglobin (Hb), whose incorporated iron can act as
61              Intraplaque hemorrhage releases free hemoglobin (Hb).
62     Nitric oxide (NO) is inactivated by cell-free hemoglobin in a dioxygenation reaction that also ox
63 asured electrolytes, blood gases, and plasma-free hemoglobin in arterial blood, as well as blood ente
64                                   Studies on free hemoglobin in circulation have uncovered another tw
65  thereby limiting oxidative damage caused by free hemoglobin in metabolic tissues.
66 ng effects of nitrite would be attenuated by free hemoglobin in plasma that would rapidly scavenge NO
67 ikilocytosis, echinocytosis, schistocytosis, free hemoglobin in plasma, hemoglobinuria with hemosider
68 used in part by an increase in NO-scavenging free hemoglobin in the blood, by hypoargininemia, and by
69                                         Cell-free hemoglobin in the CSF of patients with aSAH disrupt
70          Treatment with haptoglobin retained free hemoglobin in the plasma and prevented SRBC-induced
71       Exogenous NO inactivated NO-scavenging free hemoglobin in the plasma and restored nitrite to co
72 e dynamics could be enhanced by elevation of free hemoglobin in the plasma, which occurs in diseases
73                  Acetaminophen inhibits cell-free hemoglobin-induced lipid peroxidation and improves
74 cial in sepsis, including inhibition of cell-free hemoglobin-induced oxidation of lipids and other su
75 y exert a protective effect by reducing cell-free hemoglobin-induced oxidative injury.
76                                       Plasma free hemoglobin is elevated in SCD patients and acutely
77 centration (r = -0.45, P = .002), and plasma-free hemoglobin level (r = -0.41, P = .01), linking eryt
78 cetaminophen by prerandomization plasma cell-free hemoglobin level higher than 10 mg/dL.
79  was no significant interaction between cell-free hemoglobin levels and acetaminophen.
80 h the infusion of microspheres increase cell-free hemoglobin levels and nitric oxide consumption by p
81  in vitro tests, researchers measured plasma-free hemoglobin levels in a 36-year-old man to assess me
82    Erythrocyte ATP, 2,3-DPG, hemoglobin, and free hemoglobin levels in the supernatant were determine
83                                              Free hemoglobin levels increased in all patients but did
84 lene conjugate (8% PHP [n = 9], or 8% stroma-free hemoglobin (n = 7).
85 red include platelet activation, toxicity of free hemoglobin, nitric oxide depletion, absence of othe
86 hepatocytes in dogs resuscitated with stroma-free hemoglobin or PHP.
87 lyze in vivo, releases vasoconstrictive cell-free hemoglobin over days, worsens pulmonary hypertensio
88 of products in development are based on cell-free hemoglobin, perfluorocarbon emulsions, or liposome-
89                                  Mean plasma free hemoglobin (pfHb) increased from 26.45 to 76.00 mg/
90 d ratio antithrombin III, fibrinogen, plasma-free hemoglobin, platelets, and decline in D-dimer <= 50
91 thologically relevant concentrations of cell-free hemoglobin promoted basal- and agonist-stimulated a
92 , which is associated with microparticle and free hemoglobin release, and age-related loss of enzymat
93 CPB leads to the generation of intravascular free hemoglobin, resulting in increased endothelial and
94                                         Cell-free hemoglobin's (CFH) high affinity for nitric oxide (
95 observed upon exchange transfusion with cell-free hemoglobin solutions can not be the result of .NO s
96                                    Many cell-free hemoglobin solutions designed as oxygen-carrying th
97 pport the conclusion that the PHP and stroma-free hemoglobin solutions tested did not produce hepatic
98 eacts at least 1,000 times more rapidly with free hemoglobin solutions than with erythrocytes.
99 s release of both membrane vesicles and cell free hemoglobin that in turn initiates vaso-occlusive ev
100                                         Cell-free hemoglobin that is released from erythrocytes into
101   Haptoglobin is a plasma protein that binds free hemoglobin, thereby inhibiting hemoglobin-induced o
102                Whole blood viscosity, plasma free hemoglobin, TR jet, and FMD were measured in chroni
103 ith severe sepsis and detectable plasma cell-free hemoglobin, treatment with acetaminophen within 24
104 , 10% pentastarch (one of seven), and stroma-free hemoglobin (two of seven) and was accompanied by an
105 t elevated in those with malaria, and plasma free hemoglobin was elevated only in patients with cereb
106  50-min period; and c) a group in which cell-free hemoglobin was exchanged transfused to reduce hemat
107  of intracellular ATP and 2,3-DPG levels and free hemoglobin was increased in the supernatant.
108 etaminophen in the setting of increased cell-free hemoglobin was independently associated with a prot
109 d using reductive chemiluminescence and cell-free hemoglobin was measured with a colorimetric assay.
110                                  Plasma cell-free hemoglobin was weakly correlated with plasma NO con
111 from blood samples containing PHP and stroma-free hemoglobin were made.
112 me (APTT), heparin concentration, and plasma free hemoglobin were obtained before, during, and after
113 going red cell breakdown and release of cell-free hemoglobin, which together contribute to a number o
114     In vitro interferences of PHP and stroma-free hemoglobin with liver function tests were determine
115 , and some have postulated release of plasma-free hemoglobin with subsequent nitric oxide consumption
116                    We postulated that plasma free hemoglobin would be negatively associated with both

 
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