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1 e posed an experimental challenge to measure blood viscosity.
2 good agreement with in-vitro measurements of blood viscosity.
3 on blood flow and the estimates of effective blood viscosity.
4 ions with both fibrinogen concentrations and blood viscosity.
5  cell measures is probably mediated by whole blood viscosity.
6         Hematocrit is a determinant of whole blood viscosity.
7 xygen concentration without risking elevated blood viscosity.
8 re and vascular shear stresses, despite high blood viscosity.
9 ing morphology exhibited the highest average blood viscosity.
10 unt and leukocytosis, resulting in increased blood viscosity.
11  the resulting changes in RBC biophysics and blood viscosity.
12 f RBCs emerges as the primary determinant of blood viscosity.
13  predicted a reduction in local and apparent blood viscosity after isovolemic hemodilution.
14  us to investigate the variation of apparent blood viscosity along the cross-section of a vessel.
15 e, we will review hemorheology, particularly blood viscosity along with other hemorheological factors
16 ried individuals and how haemoconcentration, blood viscosity and cell deformability affect blood flow
17                          Therefore, elevated blood viscosity and hematocrit deserve attention as emer
18 nown predictors of diabetes, estimated whole blood viscosity and hematocrit predicted incident type 2
19          These findings suggest that in men, blood viscosity and its major determinants are associate
20 g of how changes in RBC properties impact on blood viscosity and may affect bone health, offering a p
21 ing hyperlipidemia is secondary to increased blood viscosity and not abnormal coronary vasomotion.
22 iated with hyperlipidemia is due to increase blood viscosity and not abnormal vascular function.
23 may be "downregulated." This may lower whole blood viscosity and partially reduce DBP without comprom
24 e to factors such as mean arterial pressure, blood viscosity and pH.
25 s a significant negative association between blood viscosity and the mean flow velocity in the middle
26 not directly related to alterations in whole blood viscosity and the shear stimulus.
27 comes, including oxidative stress, increased blood viscosity, and impaired systemic response to infla
28 asound), arterial blood gases, Hct and [Hb], blood viscosity, and NO metabolites (ozone-based chemilu
29 iscosity (P< or =.01), fibrinogen, corrected blood viscosity, and plasma viscosity (all P< or =.05).
30 uclear neutrophil; PMN) deformability, whole-blood viscosity, and platelet-neutrophil interactions on
31 both RBC aggregation and stiffness impact on blood viscosity; and the stiffness domain, where the sti
32                  Other major determinants of blood viscosity are hematocrit, level of inflammatory pr
33 r and tissue pressures and/or an increase in blood viscosity as a result of increased hematocrit.
34 an additional mechanism of increased in vivo blood viscosity as compared to that determined in vitro.
35              Its width affects the effective blood viscosity as well as the scavenging and production
36 confirmed fibrinogen's substantial impact on blood viscosity at low shear rates in the LAA, suggestin
37  results reveal three distinct domains of GD blood viscosity based on shear rate: the aggregation dom
38 duced Hct by 18 +/- 2% (P < 0.001) and whole blood viscosity by 22 +/- 5% (P < 0.001).
39 , we investigated the feasibility to monitor blood viscosity by electrical bioimpedance in 10 patient
40                    Excessive haematocrit and blood viscosity can increase blood pressure, cardiac wor
41 aemoglobin mass, blood and plasma volume and blood viscosity, cardiac output, blood pressure and chan
42                     Instead, the increase in blood viscosity causes capillary resistance to rise, whi
43  data (immunoglobulin level, hematocrit, and blood viscosity), clinical examination results, and OCT
44 sure, decreased cardiac output and increased blood viscosity combine to diminish venous return.
45 monstrates the proof of principle to monitor blood viscosity continuously in the human right atrium b
46    The M-protein and the related increase in blood viscosity could be a novel etiologic discovery for
47                                              Blood viscosity decreases with shear stress, a property
48                                 Furthermore, blood viscosity, fibrinogen (both P< or =.01), and plasm
49  bulk modulus of the ruptured wall material, blood viscosity, flow rate and mass density of the monoc
50 r the non-linear regression model estimating blood viscosity from its major determinants hematocrit a
51 quartiles, adults in the highest quartile of blood viscosity (hazard ratio = 1.68, 95% confidence int
52 s showed fibrinogen significantly influenced blood viscosity in all AF cohorts.
53 aggregation threshold, and cell stiffness on blood viscosity in GD.
54   By analyzing RBC mechanical properties and blood viscosity in relation to bone disease, we find tha
55                                 High average blood viscosity in the LAA of atrial fibrilation + Covid
56       Fibrinogen has a significant effect on blood viscosity in the left atrial appendage (LAA) at lo
57                                   Changes in blood viscosity in vivo are associated with changes in f
58 evels with the potential risks of increasing blood viscosity, in the context of the current therapeut
59                                              Blood viscosity increased significantly as temperature d
60     Hemorheologic analyses revealed enhanced blood viscosity, increased aggregation, and disaggregati
61                                              Blood viscosity is an important determinant of microvasc
62 of evidence support the notion that elevated blood viscosity may predispose to insulin resistance and
63 C aggregation properties, deformability, and blood viscosity, may contribute to its onset.
64                                              Blood viscosity, or the resistance of flow, can be alter
65                                      In men, blood viscosity (P< or =.001) and its major determinants
66 s distribution (1.05 mm) for SD increases in blood viscosity (P< or =.01), fibrinogen, corrected bloo
67                                        Whole blood viscosity, plasma free hemoglobin, TR jet, and FMD
68                                        Whole blood viscosity, plasma viscosity, hematocrit, and fibri
69 nse relationship with fibrinogen, plasma and blood viscosity, platelet count, coagulation factors VII
70                             Considering that blood viscosity plays an important role in cerebral bloo
71                                              Blood viscosity provides the rheological basis to elucid
72  noted between serum triglyceride levels and blood viscosity (r=0.82).
73 ifferences in mean arterial pressure, pH and blood viscosity, race accounts for an approximately 100
74                      Radial distributions in blood viscosity, shear stress, and shear rate are obtain
75                                          The blood viscosity-shear rate relationship was obtained fro
76 This model explains 89.2% (R(2)=.892) of the blood viscosity-shear rate relationship.
77 t than DM patients and had an elevated whole blood viscosity that correlated with plasma glucose (p =
78 gregation threshold predominantly influences blood viscosity; the transition area, where both RBC agg
79  stimulates platelet function, and increases blood viscosity through hemoconcentration.
80                                   Correcting blood viscosity to a standard hematocrit of 45% had litt
81                                 Reduction of blood viscosity via gata1a morpholino oligonucleotides (
82 n the following equation to estimate in-vivo blood viscosity (Viscosity(imp)) from plasma resistance
83 l configuration, the experimentally acquired blood viscosity was compared with a vacuum-driven capill
84                                        Whole blood viscosity was estimated by using a validated formu
85                       At baseline, estimated blood viscosity was independently associated with severa
86 dynamics, myocardial blood flow (MBF), whole blood viscosity (WBeta), erythrocyte charge (EC) and mob
87                                        Whole blood viscosity (WBV) is a clinically validated measure
88                        To determine if whole blood viscosity (WBV), a rheologic variable contributing
89 with reduced cell deformability and elevated blood viscosity, which contribute to impaired blood flow
90 in Experiment 1 is associated with increased blood viscosity, which is an important factor affecting
91 ry high hemoglobin concentrations cause high blood viscosity, which results in both compromised oxyge
92 pression by nitrate may thus act to decrease blood viscosity while matching oxygen supply to demand,
93 red blood cell volume, caused an increase in blood viscosity yet similar total blood volume.