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The Rational Basis of Thrombosis Models
Published in Josef Hladovec, Antithrombotic Drugs in Thrombosis Models, 2020
Of the various tests available for the estimation of the rheologic properties of blood, it is necessary to name hematocrit, fibrinogen estimation, and to some extent, even the sedimentation rate. A more objective method is viscosity estimation at various shear rates. Rotation viscosimeters are generally used for this purpose. Erythrocyte deformability may be determined by various methods such as the filtration rate or viscosity measurement at relatively higher shear rates with whole blood and plasma. None of these deformability methods is adequately standardized.
Erythrocyte Deformability
Published in Gordon D. O. Lowe, Clinical Blood Rheology, 2019
This chapter was written to emphasize the importance of determinants of erythrocyte deformability when designing, or evaluating, any clinical study with an acquired abnormality of erythrocyte deformability. Other design principles for clinical and laboratory studies of erythrocyte deformability have been described elsewhere140 and the International Committee for Standardization in Haematology has recently published guidelines on rheological measurements.141 When a rheological abnormality is demonstrated, it is important, first, to exclude artifacts arising from factors extrinsic to the erythrocyte (e.g., leukocytes, plasma proteins, and inappropriate buffer), and then to determine which factors intrinsic to the erythrocyte (e.g., MCV, MCHC, and shape change) have contributed to the loss of deformability. The role of these factors, both extrinsic and intrinsic, should always be commented on by authors when interpreting the results of rheological studies. Since more than one intrinsic determinant may contribute to loss of erythrocyte deformability, and since different rheological instruments show differing sensitivity to these determinants, a combination of instruments is required to provide maximum rheological information.
Rheology of Diabetes Mellitus
Published in Gordon D. O. Lowe, Clinical Blood Rheology, 2019
Erythrocyte deformability might be impaired in diabetes because of changes in the intracellular hemoglobin, changes in the physical properties of the cell membrane, or changes in the surface area to volume ratio of the cells (Chapter 4, Volume I). Hemoglobin A1, a, b, and c concentrations are increased in diabetics, particularly during poor metabolic control. Although Boudart et al.32 have found no differences in the viscosity of solutions containing varying amounts of glycosylated hemoglobins, it remains possible that HbA,c binds more avidly to the red cell membrane,41,95 with deleterious effects on its flexibility.
Could hemogram parameters be predictors of dementia in elderly patients?
Published in The Aging Male, 2019
Erythrocyte deformability, which makes erythrocytes able to change their morphology during transition through small vessels, is crucial for maintaining microcirculation and oxygen supply of the tissues. Increased RDW is considered as a marker of erythrocyte deformability [26]. Erythrocytes with reduced deformability may cause deterioration of blood flow in capillaries [27]. Such blockage in cerebral vessels may cause leukoaraiosis and increased Fazekas’s scores in imaging studies. However, it is not clear whether elevated RDW is a cause of leukoaraiosis or it is a consequence of that pathological condition.
The relationship between red cell distribution width and the risk of Henoch–Schönlein purpura nephritis
Published in British Journal of Biomedical Science, 2018
X Zhu, M Zhang, F Lan, H Wei, Q He, S Li, X Qin
At present, the precise pathogenesis behind the relationship between RDW and HSPN is unknown. Some studies have shown that RDW may be influenced by inflammatory factors, including IL-6 and TNF-α [24]. Inflammatory cytokines may influence the function of bone marrow and suppress the maturation of erythrocytes, leading to increased RDW values [27]. Thus, higher RDW values could reflect an underlying inflammatory state caused by chronic inflammation that could in turn transform erythrocyte homeostasis and impair erythrocyte maturation [28]. The pathogenesis of HSPN may also be accounted for by inflammatory conditions. Chang et al. [29] has reported that the overexpression of IL-17, IL-4 and IFN-γ contributes to the onset of HSP. Xu et al. [3] has also found that one single-nucleotide polymorphism of IL-17A gene is a risk factor for HSP and that IL-17A has an important function in the pathogenesis of HSP. Furthermore, Ding et al. [30] established that TNF-α (+308G/A) gene polymorphisms are associated with HSP in children. These findings indicate that inflammatory reactions contribute to the pathogenesis of HSPN. On the other hand, some reports have suggested that a decline in erythropoietin (EPO) contributes to the risk of renal injury [31,32]. EPO hyporesponsiveness could reduce the production of RBCs by promoting bone-marrow production and maturation and erythrocyte survival, hence elevating RDW [33,34]. Gurses et al. [35] have suggested that reduced erythrocyte deformability increases the risk of renal involvement. Patel et al. [36] have reported that elevated RDW is significantly correlated with decreased erythrocyte deformability. These data suggest that the robust relationship between RDW and a state of inflammatory conditions, a decline in EPO or erythrocyte deformability may explain why the RDW levels increased in the HSP and HSPN patients in this study.
Hemorheological dysfunction in cardiac syndrome X
Published in Acta Cardiologica, 2018
Emine Kilic-Toprak, Olga Yaylali, Yalin Tolga Yaylali, Yasin Ozdemir, Dogangun Yuksel, Hande Senol, Tarık Sengoz, Melek Bor-Kucukatay
Another hemorheological parameter determined in the current study is the erythrocyte deformability. Normal erythrocytes are highly deformable and this issue greatly facilitates blood flow in the narrow channels of the circulation [5,10]. The inability to deform would make it difficult for the red cells to perform their function of oxygen delivery and RBCs with reduced deformability are removed from the circulation by the reticuloendothelial system. Thus, significant decreases in RBC deformability compromises blood flow through the microcirculation and curtails nutrient support [5,10]. Although up to our knowledge, it is not still clear how much alteration in RBC deformability has clinical meaning; similar to our results, impairments in RBC deformability have been reported in a number of cardiovascular diseases, including myocardial infarction [40], hypertension [41] and chronic heart failure [31]. Erythrocyte deformability was measured between 0.3 and 16.87 Pa, representing the shear stresses erythrocyte encounters at different sites of circulation and was found to be lower at 1.69 and 3.00 Pa in CSX. The shear stress level of normal coronary arteries was demonstrated to be around 2 Pa [42]. This information increases the importance of the reduced RBC deformability determined at 1.69 and 3 Pa in CSX herein. The relations between pressure and blood flow become more complex in the microcirculation as the vessel diameter approaches average RBC size. RBC distribution at precapillary branch points is strongly affected by local blood rheology, and both Hct and blood viscosity decrease with decreasing vascular diameter [23]. Enhanced RBC aggregation leads to reduced microvascular blood flow and, in addition, promotes the axial accumulation of erythrocytes, leaving a cell poor plasma layer with lower viscosity adjacent to the vascular endothelium [10,29]. As a consequence, shear stress decreases at the vessel wall, thus reducing nitric oxide synthesis that is already suppressed in individuals with CSX [43]. It is known that, erythrocyte deformability is affected by membrane skeleton elasticity, cytoplasmic viscosity and cell geometry (surface-volume ratio) [10,29]. In our study, MCHC values in CSX patients were lower when compared to those of the controls. Decreased deformability is usually associated with, increment of MCHC, which is not true in our case. Thus, deformability alterations may not be explained by MCHC changes herein. Impaired deformability also makes erythrocyte life span shorter which may be related with the increment observed in RDW [44].