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PubMedDate not supplied

Flow behavior of erythrocytes in microvessels and glass capillaries: effects of erythrocyte deformation and erythrocyte aggregation.

Flow behavior of erythrocytes in microvessels and glass capillaries with an inner diameter of 10-50 microns was compared in relation to erythrocyte deformation and erythrocyte aggregation. This study was focused on the formation of a marginal cell-free layer, and the thickness was determined using an image processor. Human erythrocytes were perfused through a part of microvascular networks isolated from rabbit mesentery and through glass capillaries. Erythrocyte deformability was modified by treating erythrocytes with diamide, diazene-dicarboxylic acid bis[N,N-dimethylamide], and erythrocyte aggregation was accelerated by adding dextran (with a molecular weight of 70,400) to the perfusion medium. The thickness of the cell-free layer increased with an increase of the inner diameter of flow channel, with lowering the hematocrit, and with increasing the flow velocity of erythrocytes, in both microvessels and glass capillaries. Furthermore, the thickness of cell-free layer decreased with decreasing erythrocyte deformability, while it increased with accelerating erythrocyte aggregation. However, the alteration of the cell-free layer in response to the changes of these hemorheological conditions was more sensitive in microvessels than in glass capillaries. The present study concludes that flow behavior of erythrocytes in microvessels is qualitatively similar to, but quantitatively different from those in glass capillaries, as far as evaluated by the change of the thickness of the marginal cell-free layer.

Animals↗
PubMed2001

O(2) release from erythrocytes flowing in a narrow O(2)-permeable tube: effects of erythrocyte aggregation.

The effects of erythrocyte aggregation on O(2) release were examined using O(2)-permeable fluorinated ethylenepropylene copolymer tubes (inner diameter, 25 microm; outer diameter, 100 microm). Measurements were performed using an apparatus built on an inverted microscope that contained a scanning-grating spectrophotometer with a photon count detector connected to two photomultipliers and an image processor through a video camera. The rate of O(2) release from the cells flowing in the narrow tube was determined based on the visible absorption spectrum and the flow velocity of the cells as well as the tube size. When the tube was exposed to nitrogen-saturated deoxygenated saline containing 10 mM sodium dithionite, the flowing erythrocytes were deoxygenated in proportion to the traveling distance, and the deoxygenation at a given distance increased with decreasing flow velocity and cell concentration (hematocrit). Adding Dextran T-70 to the cell suspension increased erythrocyte aggregation in the tube, which resulted in suppressed cell deoxygenation and increased marginal cell-free-layer thickness. The deoxygenation was inversely proportional to the cell-free-layer thickness. The relation was not essentially altered even when the medium viscosity was adjusted with Dextran T-40 to remain constant. The rate of O(2) release from erythrocytes in the tube was discussed in relation to the O(2) diffusion process. We conclude that the diffusion of O(2) from erythrocytes flowing in narrow tubes is inhibited primarily by erythrocyte aggregation itself and partly by thickening of the cell-free layer.

Diffusion↗
PubMed2002

Involvement of fibrinogen specific binding in erythrocyte aggregation.

Increased fibrinogen concentration and erythrocyte aggregation are significant risk factors during various cardiovascular diseases and cerebrovascular disorders. Currently, fibrinogen-induced erythrocyte aggregation is thought to be caused by a non-specific binding mechanism. However, the published data on changes in erythrocyte aggregation during hypertension point to the possible existence of other mechanism(s). Therefore, we tested the hypothesis that specific binding of fibrinogen is involved in erythrocyte aggregation. It was found that Oregon Green 488-labeled human fibrinogen specifically binds rat erythrocyte membranes with a Kd of 1.3 microM. Further experiments showed that the peptide Arg-Gly-Asp-Ser blocked both fibrinogen-induced aggregation of intact erythrocytes and specific binding of fibrinogen to the erythrocyte membranes. These results suggest that in addition to non-specific binding, a specific binding mechanism is also involved in fibrinogen-induced erythrocyte aggregation.

Animals↗
PubMed1999

Erythrocyte-aggregating relapsing fever spirochete Borrelia crocidurae induces formation of microemboli.

The African relapsing fever spirochete Borrelia crocidurae forms aggregates with erythrocytes, resulting in a delayed immune response. Mice were infected with B. crocidurae and monitored during 50 days after infection. Spirochetes were observed extravascularly at day 2 after infection. Two days later, inflammatory responses, cell death, and tissue damage were evident. The pathologic responses in lungs and kidneys were similar, whereas the symptoms in the brains were delayed, with a less pronounced inflammatory response. Microemboli were found in the blood vessels, possibly a result of the erythrocyte aggregation. The B. crocidurae invasion emerged more rapidly than has been described for Lyme disease-causing Borrelia species. In addition to erythrocyte rosetting, the presence of extravascular B. crocidurae indicates a novel route for these bacteria to propagate and cause damage in the mammalian host. The histopathologic findings in this study may explain the clinical manifestations of human relapsing fever.

Animals↗
PubMed1978

[Erythrocyte aggregation and fibrinogen derivatives in ischemic heart disease].

Aggregation of erythrocytes was determined in 50 patients with angina pectoris and myocardial infarction and in 20 subjects of the control group by rheoscopy after Schmid-Schoenbein. It is shown that in patients with ischemic heart disease aggregation of erythrocytes is considerably increased and the hydrodynamic strength of the aggregates is greater. The erythrocyte aggregation curve is some patients with ischemic heart disease was of a biexponential character in distinction to that in subjects of the control group, which was of the monoexponential type. It was found that the increase in the strength of the erythrocyte aggregation and in the rate of aggregate formation was due to fibrinogen and its complex compounds with decomposition products.

Adult↗
PubMed1990

[Increase of erythrocyte aggregation in retinal vein occlusion].

Erythrocyte aggregation is one of the principal determinants of blood viscosity at low shear rates (low flow). Anatomical and hemodynamical characteristics make retinal venous circulation particularly dependent on hemorheological factors. Erythrocyte aggregation and other laboratory parameters (haematocrit, fibrinogen, plasma proteins, clotting) were measured in 85 patients presenting with retinal vein occlusion and 64 controls matched for age, sex and vascular risk factors (hypertension, diabetes, smoking). Statistical analysis of the results demonstrated a significant difference between the retinal vein occlusion group an the control group for erythrocyte aggregation (p less than 0.001 for the aggregation index at 10 sec and for the threshold of dissociation). The fibrinogen level, haematocrit and plasma proteins (albumin, IgA, IgG, IgM, total proteins, 2-macroglobulin) were similar in the two groups. No statistically significant difference for erythrocyte aggregation was observed between occlusions of the venous branch and occlusions of the central retinal vein or between ischaemic and non-ischaemic forms. These results suggest that raised erythrocyte aggregation mainly explains the increase in blood viscosity previously demonstrated, and could play a role in the constitution of retinal vein occlusion.

Acute Disease↗
PubMed1991

Effects of ticlopidine on erythrocyte aggregation in thrombotic disorders.

The authors investigated the involvement of red blood cell aggregation in thrombosis by comparing erythrocyte aggregation in patients with myocardial infarction (28 patients) or cerebrovascular accidents (68 patients) with that in a normal control group (38 subjects). The erythrocyte aggregation was assessed by light transmission aggregometer, and aggregation was induced by hexadimethrine-bromide. Increased erythrocyte aggregation was detected in all patients with thrombotic disorders. In addition, patients with diabetes mellitus showed a marked increase in erythrocyte aggregation as compared with those without diabetes. The effect of ticlopidine on erythrocyte aggregation was also studied. It was demonstrated that ticlopidine inhibited aggregation in vitro. An inhibitory effect was shown to be dose dependent, with 10 microM ticlopidine inhibiting aggregation completely. After four weeks' oral administration of 200 mg ticlopidine, there was significant decrease of abnormally increased erythrocyte aggregation in patients with thrombosis.

Aged↗
PubMedDate not supplied

Sequential analysis of erythrocyte aggregation in health and diseases.

Aggregation of erythrocytes requires prolonged interaction of cellular and plasma constituents similar to in vivo conditions. To achieve this and then to analyse this process in various clinical and laboratory conditions, a PC-AT based system is developed. The erythrocyte suspension at 5% hematocrit in plasma is placed in a glass chamber, and the changes in laser transmitted intensity due to movement of the aggregates and erythrocytes in the path of the beam are sequentially recorded. From these data, aggregate size index, aggregate sedimentation time index, time required for completion of process and total number of fluctuations are calculated. From these, two additional parameters - effective number of cells and effective sedimentation duration - are calculated. The results show that in leprosy the aggregation of erythrocytes is reduced. In in vitro studies due to the cholesterol-enrichment of the erythrocyte membrane and treatment with pentoxifylline the aggregation of cells is increased whereas in disprin treated cells this is reduced compared to that of normal erythrocytes.

Erythrocyte Aggregation↗
PubMed1981

[Effect of polyethylene oxides on erythrocyte aggregation].

The effect of polyethylene oxide of different molecular weight on the aggregation of erythrocytes has been investigated. It was shown that the addition to blood of polymers with molecular weight of 600 and 1 000 weakens this aggregation, whereas the addition of those with molecular weights of 4 000 and 6 000 completely prevents it, simultaneously decreasing their osmotic resistance. Polyethylene oxide with molecular weight from 20 000 to 1 000 000 increase the aggregation of erythrocytes and do not affect their osmotic resistance. The aggregation of erythrocytes is a reversible process. The decrease in polyethylene oxide concentration leads to decreasing aggregation effect. The mechanism of the effect of polymers on cell aggregation is discussed.

Animals↗
PubMed2006

Hemorheologic abnormalities associated with HIV infection: altered erythrocyte aggregation and deformability.

PURPOSE: To investigate possible alterations of erythrocyte aggregation and deformability, which are factors that can influence blood flow, in human immunodeficiency virus (HIV)-infected individuals and to determine whether these factors are related to the severity of immunodeficiency. METHODS: Laboratory evaluations were performed on 46 HIV-infected individuals and 44 HIV-negative control subjects. Current and nadir (lowest previous) CD4+ T-lymphocyte counts were identified for each subject. Erythrocyte aggregation was measured using a fully automatic erythrocyte aggregometer. Factors related to erythrocyte aggregation were also determined: erythrocyte sedimentation rate (ESR), zeta sedimentation ratio (ZSR), and plasma fibrinogen levels. Erythrocyte deformability was observed at various fluid shear stress levels, with a laser diffraction ektacytometer. Correlations were sought between each of these measures and current or nadir CD4+ T-lymphocyte counts, and each measure was compared between three subgroups based on current and nadir CD4+ T-lymphocyte counts (severely immunosuppressed, immune reconstituted, never severely immunosuppressed). RESULTS: The following parameters were significantly different between HIV-infected subjects and controls: increased erythrocyte aggregation, at stasis (P < 0.001) and low shear stress (P < 0.001), increased ESR (P < 0.001), increased ZSR (P < 0.028), increased serum fibrinogen (P = 0.015), and decreased erythrocyte deformability (P < 0.001). Only erythrocyte aggregation at stasis correlated significantly with current CD4+ T-lymphocyte count (r = - 0.344, P = 0.022). None of the parameters was significantly different between HIV-infected subgroups. CONCLUSIONS: Increased aggregation and decreased deformability of erythrocytes are associated with HIV-infection regardless of the severity of immunodeficiency. HIV-infected individuals may be at risk for progressive retinal microvascular damage from persistent hemorheologic abnormalities, despite immune reconstitution associated with potent antiretroviral drug therapies.

Adult↗
PubMed1983

[Characteristic features of erythrocyte aggregation in different animals and in man].

The reversible erythrocytes aggregation is considered to be a basic microrheological process determining a number of microcirculation features. But the problem of the adaptive role of erythrocytes aggregation still needs elucidation. The markedness of erythrocytes aggregation was compared in mammals occupying different positions in the evolutionary systematics: in 62 animals of 10 species and in 25 healthy humans. The species features of the erythrocytes aggregation were altered by means of adding high--molecular polyoxyethylene to blood plasma. The data obtained gave evidence on species differences in the erythrocytes aggregation, specifics of cell membrane, differences in the latter's electrostatic charge.

Animals↗
PubMed1993

[Erythrocyte aggregation in the blood in different states of the animal organism].

Aggregation of erythrocytes in the blood of rabbits was shown to depend on concentration of proteoglycans in the blood plasma. In experimental sepsis (Str. haemolyticus) there occurred simultaneous increase of concentration of proteoglycans in plasma and increased aggregation of erythrocytes in the blood. In pregnancy, the concentration of proteoglycans in the blood was constant at a low level throughout the period of pregnancy.

Animals↗
PubMed1983

[Statistical study on the effect of erythrocyte aggregation on blood filterability].

The values of erythrocyte aggregation (expressed as erythrocyte sedimentation rate corrected for plasma viscosity and hematocrit) were correlated with the values of blood filterability in a group of 165 healthy subjects and patients suffering for the most part from vascular disorders. A highly significant inverse correlation (r = -0.57, p less than 0.001) was observed between the two parameters, being a lower blood filterability correlated with a higher erythrocyte aggregation.

Arterial Occlusive Diseases↗
PubMed1992

Nifedipine treatment in preeclampsia reverts the increased erythrocyte aggregation to normal.

OBJECTIVES: Our objectives were to assess erythrocyte aggregation in hypertensive pregnancy and to evaluate the effect of the antihypertensive treatment on it. STUDY DESIGN: The mean entity of erythrocyte aggregation was determined by an automatic aggregometer in 57 pregnant women: 20 normotensive, seven chronically hypertensive, 10 chronically hypertensive with superimposed preeclampsia, and 20 with preeclampsia. Ten of the latter were subsequently treated by 40 mg/day oral nifedipine; the other 10 by 400 mg/day oral labetalol, to keep diastolic blood pressure < 90 mm Hg. Also, patients with superimposed preeclampsia were treated with 40 mg/day oral nifedipine. RESULTS: Erythrocyte aggregation was increased in all the hypertensive pregnant patients compared with the normotensive pregnant controls, regardless of both the onset (chronic or pregnancy-induced) of hypertension and the status of plasma macromolecules. Antihypertensive treatment with labetalol significantly reduced the aggregability of erythrocytes, whereas treatment with nifedipine reverted it to normal. CONCLUSIONS: Increased erythrocyte aggregation may be due to either conformational changes of the membrane occurring during hypertension or a redistribution of the ionic charges on the two surfaces of the membrane. The effect of nifedipine by restoring the ionic charges may be due to this latter event.

Erythrocyte Aggregation↗
PubMed1976

[Thrombocyte and erythrocyte aggregation in congestive circulatory insufficiency].

In 58 patients with Stage II-III congestive circulatory insufficiency photometric techniques permitted to reveal an increased aggregation of platelets and erythrocytes. The increased erythrocytes aggregation in congestive circulatory insufficiency correlated with an increased sodium content in the erythrocytes (r = +0,82) and total body content of water (r = +0,62). The mechanisms of increased platelets and erythrocytes aggregation are discussed, as well as their role in microcirculation disorders observed in circulatory insufficiency.

Adult↗
PubMed1992

Decrease in erythrocyte glycophorin sialic acid content is associated with increased erythrocyte aggregation in human diabetes.

1. Sialic acid moieties of erythrocyte membrane glycoproteins are the principal determinants of the negative charge on the cell surface. The resultant electrostatic repulsion between the cells reduces erythrocyte aggregation and hence the low shear rate viscosity and yield stress of blood. 2. Using g.c.-m.s., a decrease in sialic acid content has been observed in the major erythrocyte membrane glycoprotein, glycophorin A, obtained from nine diabetic patients compared with that from seven normal control subjects [median (range): 3.30 (0.01-11.90) versus 18.60 (3.20-32.60) micrograms/100 micrograms of protein, P less than 0.02]. 3. Erythrocyte aggregation, measured by viscometry as the ratio of suspension viscosity to supernatant viscosity (LS/S) in fibrinogen solution, was increased in ten diabetic patients compared with ten normal control subjects (mean +/- SEM, 37.6 +/- 1.3 versus 33.8 +/- 0.6, P less than 0.02). 4. In the patients in whom both viscometry and carbohydrate analysis were performed, the decrease in erythrocyte glycophorin sialylation and the increase in erythrocyte aggregation in fibrinogen solution were related statistically (LS/S correlated negatively with glycophorin sialic acid content, r = 0.73, P less than 0.05). 5. Decreased glycophorin sialylation provides an explanation at the molecular level for increased erythrocyte aggregation and it may be important in the pathogenesis of vascular disease in diabetes.

Adult↗