[Erythrocyte aggregation, erythrocyte filterability and membrane fluidity in single-area atherosclerotic vascular disease].
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Arteriosclerosis↗
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Results for “Erythrocyte Aggregation”
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Influence of naftidrofuryl, a serotonergic antagonist, on erythrocyte aggregation.
Erythrocyte aggregation is an important determinant of the rheological behavior of blood and may play a critical role in nutritive tissue perfusion at the level of the microcirculation, particularly in situations of low flow. Thus, abnormal red blood cell aggregation may contribute to the pathophysiology of a variety of vascular diseases with associated microcirculatory disturbances. The action of serotonergic antagonists has a hemorheological component, although red blood cell aggregation specifically has not been addressed previously. Therefore, the effect of naftidrofuryl, a 5-hydroxytryptamine-2 receptor antagonist (5-HT2), on erythrocyte aggregation was studied in whole blood obtained from adult human volunteers. Red blood cell aggregation was measured using a Myrenne aggregometer the operation of which is based on nephelometric principles. The results demonstrate that red blood cell aggregation is significantly reduced in comparison to controls on incubation of whole blood in the presence of naftidrofuryl. This inhibitory effect is concentration dependent and reaches a maximum (approximately 30%) between 1 and 10 microM naftidrofuryl. Furthermore, naftidrofuryl (5 microM) also inhibits red blood cell aggregation in the presence of exogenously added serotonin (1 microM) on average by approximately 18%. Significant inhibition of red blood cell aggregation could not be observed in similar experiments using whole blood suspensions essentially devoid of platelets, suggesting that these blood cellular elements are involved in mediating the effects of naftidrofuryl.
Adult↗
Approach to erythrocyte aggregation through erythrocyte sedimentation rate: application of a statistical model in pathology.
Erythrocyte sedimentation rate (ESR) is mainly used in clinical practice as a screening test for inflammatory diseases and sometimes in the follow-up of patients. However, ESR is highly dependent on erythrocyte aggregation. In this study, using a Sediscan (Becton) automatic device measuring the kinetics of ESR, these results are compared with the measurement of erythrocyte aggregation as determined by laser light backscattering (Erythroaggregometer Affibio). A series of 188 samples from in-patients were tested. Statistical analysis of 13 parameters indicates that 82% of ESR variance may be explained by fibrinogen level, haematocrit and a parameter characterizing erythrocyte aggregation: the aggregation index at 10 s. This correlation was then validated prospectively in 128 other patients and seems to be independent of the underlying disease. Thus ESR in combination with fibrinogen assay and haematocrit may be considered as a simple and economic method to assess erythrocyte aggregation.
Blood Sedimentation↗
Erythrocyte aggregation and erythrocyte membrane properties in type 2 diabetes mellitus and in vascular atherosclerotic disease.
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Aged↗
Involvement of erythrocyte aggregation and erythrocyte resistance to flow in acute coronary syndromes.
The objective of the study was to identify the relative importance of erythrocyte flow resistance and aggregation in acute and chronic coronary syndromes. 117 subjects in five groups were studied: (1) 34 patients shortly after acute myocardial infarction (AMI) before reperfusion therapy; (2) 27 patients with unstable and (3) 21 with stable angina pectoris (AP); (4) 14 age-matched control patients and (5) 21 healthy volunteers. Single erythrocyte transit times were measured using the Cell Transit Analyser. Shear dependent elongation and aggregation was measured by a modified computerized Myrenne aggregometer. Leukocyte count was increased in coronary artery disease (CAD), especially in acute syndromes (mean +/- SD for groups 1-5): 12.2 +/- 4.5; 10.0 +/- 5.4; 8.0 +/- 2.0; 8.0 +/- 3.7; 7.0 +/- 2.0 (pl(-1))). Platelets, hematocrit, fibrinogen, alpha2-macroglobulin did not differ between the groups. Plasma viscosity (mPas) was elevated in AMI and stable AP: 1.34 +/- 0.10; 1.30 +/- 0.09; 1.32 +/- 0.08; 1.27 +/- 0.07; 1.27 +/- 0.05. Erythrocyte filtrability was not different as was the shear dependent deformation. Aggregation parameters such as gammaTmin were elevated in CAD: 180 +/- 70; 159 +/- 60; 166 +/- 59; 115 +/- 43; 113 +/- 51 (s(-1)). Erythrocyte deformability, measured with two independent methods, does not appear to contribute to the pathophysiology of acute coronary syndromes. Erythrocyte aggregation and plasma viscosity were again found increased both in unstable and stable coronary disease. It is unlikely that increased red cell aggregation contributes to emergence of AMI.
Acute Disease↗
Fibrinogen-induced erythrocyte aggregation: erythrocyte-binding site in the fibrinogen molecule.
The effect of fibrinogen and fibrinogen-derived products on the velocity of rouleau formation of human erythrocytes was quantitatively examined with a rheoscope combined with a video-camera, an image analyzer and a computer. (i) The velocity of rouleau formation by naturally occurring low-molecular-weight fibrinogen of 305 kDa and by desialylated fibrinogen was the same as that by native fibrinogen of 340 kDa. (ii) Concerning fibrinogen degradation products by plasmin, the velocity of rouleau formation decreased upon going from fibrinogen greater than fragment X greater than fragment Y (the ratio of molar concentration of fibrinogen, fragment X and fragment Y for giving a certain velocity of rouleau formation was approx. 1:2:5). The effect of fragments X and Y on the fibrinogen-induced rouleau formation was additive. (iii) Fragments D and E could not induce rouleau formation and did not affect the fibrinogen-, fragment X- and fragment Y-induced rouleau formation. (iv) Fibrinopeptides A and B and artificial tetrapeptides (Gly-Pro-Arg-Pro and Gly-His-Arg-Pro) did not affect the fibrinogen-induced rouleau formation. (v) The possible erythrocyte-binding site in fibrinogen molecule for leading to rouleaux was proposed to be in A alpha-chain (probably, around residues No. 207-303) near the terminal domain of the trinodular structure of fibrinogen.
Binding Sites↗
Erythrocyte aggregation and erythrocyte deformability modify the permeability of erythrocyte enriched fibrin network.
Intravascular thrombus formed under low shear conditions consists of red cells enmeshed within a fibrin network. Since red cells reduce the permeability of fibrin network by surface drag and by volume occupancy the significance of red cell aggregability and deformability in network permeability needs examination. In this study networks were developed by the addition of thrombin to washed red cells suspended in platelet free plasma. The effects of the polymers polyvinylpyrrolidone (PVP) and poloxamer 188 on network permeability were compared to gauge the influence of red cell aggregation. Both polymers increase network permeability by an action on fibrin polymerisation but PVP alone enhances red cell aggregation. PVP was found to increase network permeability significantly both by increasing the permeability of the fibrin component of the network and by increasing red cell aggregation and thus reducing red cell surface drag. In separate experiments red cells were pre-treated with heat, glutaraldehyde, or diamide to reduce cell deformability. Decreased cell deformability caused significant reductions in network permeability. This was ascribed to the reduced aggregability of hardened red cells. Red cell aggregation during coagulation enhances molecular transport through modifying the network. This may have implications for the penetration of fibrinolytic agents.
Blood Coagulation↗
[Erythrocyte aggregation and retinal vein occlusion. Preliminary data for a randomized study on the efficacy of anti-erythrocyte aggregation (troxerutin) in retinal vein occlusion].
Erythrocyte aggregation (EAg) is one of the principal determinants of blood viscosity at low shearing rates (slow flow). The retinal venous circulation, characterised by a slow circulatory rate and a high resistance to flow, creates a favourable environment for the formation of erythrocyte aggregates. EAg and other laboratory parameters (haematocrit, fibrinogen, plasma proteins, clotting) were measured in 64 patients presenting with retinal vein occlusion (RVO) and 64 controls matched for age, sex, risk factors (HT, diabetes, smoking) and concomitant vascular disease. Statistical analysis of the results demonstrated a significant difference between the RVO group and the control group for fibrinogen (p = 0.03) and erythrocyte aggregation (p = 0.00003 for the aggregation index at 10 sec and p = 0.0002 for the threshold of partial dissociation). The rise in the fibrinogen level alone cannot explain the increased erythrocyte aggregation. These results demonstrate that the increased EAg largely explains the hyperviscosity reported by other authors and suggest that it plays an important role in the pathogenesis of RVO.
Adult↗
Dielectric approach to investigation of erythrocyte aggregation. II. Kinetics of erythrocyte aggregation-disaggregation in quiescent and flowing blood.
A method based on dielectric properties of dispersed systems was applied to investigate the kinetics of RBC aggregation and the break-up of the aggregates. Experimentally, this method consists of measuring the capacitance at a frequency in the beginning of the beta-dispersion. Two experimental protocols were used to investigate the aggregation process. In the first case, blood samples were fully dispersed and then the flow was decreased or stopped to promote RBC aggregation. It was found that the initial phases of RBC aggregation are not affected by the shear rate. This finding indicates that RBC aggregation is a slow coagulation process. In the second case, RBCs aggregated under flow conditions at different shear rates and after the capacitance reached plateau levels, the flow was ceased. The steady-state capacitance of the quiescent blood and the kinetics of RBC aggregation after stoppage of shearing depend on the prior shear rate. To clarify the reasons for this effect, the kinetics of the disaggregation process was studied. In these experiments, time courses of the capacitance were recorded under different flow conditions and then a higher shear stress was applied to break up RBC aggregates. It was found that the kinetics of the disaggregation process depend on both the prior and current shear stresses. Results obtained in this study and their analysis show that the kinetics of RBC aggregation in stasis consists of two consecutive phases: At the onset, red blood cells interact face-to-face to form linear aggregates and then, after an accumulation of an appropriate concentration of these aggregates, branched rouleaux are formed via reactions of ends of the linear rouleaux with sides of other rouleaux (face-to-side interactions). Branching points are broken by low shear stresses whereas dispersion of the linear rouleaux requires significantly higher energy.
Adult↗
Opposite effect of albumin on the erythrocyte aggregation induced by immunoglobulin G and fibrinogen.
The effect of albumin on the immunoglobulin G (IgG)-induced and fibrinogen-induced aggregation of human erythrocytes was quantitatively examined by using a rheoscope combined with a television image analyzer and a computer. As albumin concentration in the medium was increased, the IgG-induced erythrocyte aggregation was inhibited, while the fibrinogen-induced erythrocyte aggregation was accelerated (albumin itself was not able to aggregate erythrocytes). These relations were empirically expressed by the equations, v = aG1.8/A and v = a'F1.5 (A + b'), respectively (v, the velocity of erythrocyte aggregation; A, G and F, the concentrations of albumin, IgG and fibrinogen, respectively; a, a' and b', constant). The IgG-induced erythrocyte aggregation was remarkably inhibited by the addition of poly(glutamic acid), but the fibrinogen-induced erythrocyte aggregation was not. A mechanism for the interaction of immunoglobulin G and fibrinogen with the surface of erythrocytes was proposed.
Adult↗
[Effect of polyhemoglobin composition on erythrocyte aggregation and circulation time in the vascular bed].
Aggregation of erythrocytes and circulation time of polyhemoglobins in blood plasma was estimated in the model of 50% blood loss compensation in vivo and in vitro using solutions of polyhemoglobins with different content of polymerized form (from 2-3% to 70-73%). Hemoglobin derivatives were characterized by HPLC, sedimentation analysis; the main functional properties of polyhemoglobins were evaluated as well as their influence on erythrocytes aggregation in vitro and in vivo on dogs. The optimal content of polymerized form (25-30%) was estimated which provides sufficient prolongation of circulation time and does not enhance the erythrocytes aggregation. The conclusion was made that influence on erythrocyte aggregation likewise functional properties and circulation time may be considered as criterion of optimal fractional composition and biocompatibility of the polyhemoglobins.
Animals↗
Animal species differences in erythrocyte aggregability.
Species differences in erythrocyte aggregability were investigated employing our whole blood erythrocyte aggregometer. Blood was sampled from seven species, including humans and anesthetized (30 mg/kg pentobarbital) animals. The erythrocyte aggregation rates were the following (in s-1): cats, 0.213 +/- 0.027 (means +/- SD); dogs, 0.164 +/- 0.027; men, 0.112 +/- 0.025; rats, 0.111 +/- 0.005; domestic rabbits, 0.049 +/- 0.021; and mongolian gerbils, 0.034 +/- 0.015. Domestic fowls did not exhibit erythrocyte aggregograms like those seen in the other species. Statistical analysis revealed significant differences among the erythrocyte aggregation rates of the different species (multiple-comparisons with an overall significance level of 0.05) except between men and rats and between rabbits and gerbils. No single factor which is known to accelerate the erythrocyte aggregation rate (hematocrit, fibrinogen, etc.) was correlated with the erythrocyte aggregation rate except the globulin concentration in the blood. The failure to detect erythrocyte aggregation in domestic fowls was probably attributable to their erythrocyte shape. These results suggest that each species has its own proper tendency for erythrocyte aggregation. This factor must be taken into consideration when the blood circulation is discussed among different animal species.
Animals↗
Quantitative evaluation of flow dynamics of erythrocytes in microvessels: influence of erythrocyte aggregation.
Effects of erythrocyte aggregation on the flow dynamics of erythrocytes in microvessels were examined quantitatively by perfusing human erythrocytes suspended in isotonic medium containing various concentrations of dextran (70,400 avg mol wt, Dx-70) into a part of the microvascular bed isolated from rabbit mesentery. Thickness of the marginal cell-free layer was measured with an image analyzer, total flow resistance was determined on the basis of the perfusion pressure-volume flow relationship, and homogeneity of erythrocyte flow was evaluated by the power spectrum obtained by the fast Fourier transform of the light intensity change monitored on single microvessels. With increasing dextran concentration, suspension viscosity of erythrocytes at high shear rates increased linearly and thickness of the cell-free layer increased in a sigmoidal fashion. Flow resistance increased relatively little over the range of dextran concentrations in which the cell-free layer increased most rapidly. Furthermore, the flow pattern of erythrocytes in microvessels became inhomogeneous. In conclusion, the present study shows that Dx-70-induced erythrocyte aggregation results in increased flow resistance in the circulatory system, even through the widening of the cell-free layer tends to reduce the resistance and also results in inhomogeneous flow of erythrocytes in microvessels.
Animals↗
[Reversible erythrocyte aggregation in patients with schizophrenia].
Reversible aggregation of erythrocytes was studied in 33 male patients with paranoid schizophrenia aged 23-48 years. Minimum and maximum solidity of erythrocyte aggregates, spontaneous aggregation half-period, amplitude of photometric signal, aggregation index and integral coefficient were evaluated by photometry. A significant (p < 0.001) increase of reverse aggregation of erythrocytes closely correlated with phases of schizophrenic process.
Adult↗
[Features of erythrocyte aggregation in various forms of bronchial asthma].
A model of aggregation of erythrocytes was used to study the characteristic features of membrane disorders in different forms of bronchial asthma. It was found that erythrocytic aggregations depended on the form of bronchial asthma, primarily due to the characteristic features of the erythrocytic cellular membrane. In infectious-dependent bronchial asthma and chronic obstructive bronchitis erythrocytic aggregation was increased while in atopic bronchitis it tended to decrease.
Asthma↗
Albumin affects erythrocyte aggregation and sedimentation.
Erythrocyte aggregation and sedimentation is determined by the concentration of high molecular plasma proteins such as fibrinogen and immunoglobulins. The role of albumin, the most abundant plasma protein, is controversial. We analysed the influence of human albumin (0-80 g L-1) on sedimentation behaviour of erythrocytes suspended (haematocrit 35%) in fibrinogen-enriched normal plasma, plasma from patients with hypoalbuminaemia, solutions of dextran 70 in buffer, and mixtures of fibrinogen, immunoglobulins and albumin in buffer. Sedimentation was measured by the Westergren method, viscometry was performed at low and high shear rate. The addition of albumin to normal plasma, hypoalbuminaemic plasma, or dextran solutions in buffer decreased the erythrocyte sedimentation rate. In contrast, in a mixture of fibrinogen and immunoglobulins in buffer, albumin increased erythrocyte sedimentation. When either fibrinogen or immunoglobulins were omitted, or fibrinogen was replaced by dextran, albumin did not increase sedimentation, which indicates that increased sedimentation was due to an interaction of all three compounds. The viscosity of erythrocyte suspensions was increased by albumin. It is concluded that the influence of albumin on erythrocyte aggregation is complex and depends on the technique used; low shear viscosity is increased, but erythrocyte sedimentation, i.e. under no flow conditions, is decreased. The inhibitory action of albumin on the erythrocyte sedimentation rate has clinical implications and must be known by physicians. It may help to interpret sedimentation rates more correctly and prevent misinterpreting presumed therapeutic successes or failures.
Adult↗
The significance of plasma lipoproteins on erythrocyte aggregation and sedimentation.
Increased erythrocyte aggregation can be induced by high concentrations of human lipoproteins. The dependence of aggregate formation on lipoprotein concentration was recorded by determination of erythrocyte sedimentation rate (ESR), by electrical measurement of the erythrocyte aggregation index (EAI) and by scanning electron microscopy. The lipoprotein concentrations necessary to induce a significantly increased ESR in an otherwise normal human plasma are much too high to be encountered in physiologic or even severe pathologic states. Therefore hyperlipoproteinaemia by itself cannot explain a raised ESR. In cases where the ESR is raised due to the presence of increased amounts of other erythrocyte aggregating plasma proteins (agglomerins), hyperlipoproteinaemia can contribute to a limited extent to the increase in ESR. The possible pathophysiological significance of the demonstrated erythrocyte aggregating capacity of human lipoproteins in a microvascular environment is noted.
Blood Sedimentation↗
Effect of temperature on the velocity of erythrocyte aggregation.
The velocity of the aggregation of human erythrocytes was examined in the range of 5-43 degrees C with a rheoscope combined with a video camera, an image analyzer and a computer. (1) With increasing temperature, the velocity of erythrocyte aggregation induced by fibrinogen, immunoglobulin G and artificial macromolecules (dextran of 70 kDa and poly(glutamic acid) of 50 kDa) increased. However, the relationship between the velocity of erythrocyte aggregation and the temperature was different among these macromolecules. (2) In 70% autologous plasma, the velocity of erythrocyte aggregation was minimum at 15-18 degrees C, and increased at both higher and lower temperatures. (3) The shape of erythrocyte aggregates in 12 mumol/l fibrinogen (containing 770 mumol/l albumin) and in 70% autologous plasma was dependent on temperature: three-dimensional below 15-18 degrees C and one-dimensional (mainly rouleaux) above 15-18 degrees C. However, the shape of aggregates in 27 mumol/l immunoglobulin G (containing 770 mumol/l albumin) was three-dimensional in all temperature ranges. (4) The temperature dependency of erythrocyte aggregation was discussed in terms of the changes of medium viscosity, of erythrocyte properties and of bridging macromolecules.
Adult↗