The Influence Of Red Cell Size On Platelet-Vessel Wall Interaction

1981 ◽  
Author(s):  
P A M M Aarts ◽  
J J Sixma ◽  
K S Sakariassen ◽  
P A Bolhuis ◽  
R M Heethaar
Keyword(s):  
Red Blood Cells ◽  
Cell Size ◽  
Blood Cells ◽  
Vessel Wall ◽  
Human Platelets ◽  
Red Cell ◽  
Mean Cell Volume ◽  
Human Red Blood Cells ◽  
Platelet Adherence ◽  
Order Of Magnitude

The hematocrit is one of the main factors influencing platelet adherence to the vessel wall. Raising the hematocrit causes an increase on platelet accumulation of about one order of magnitude.These studies disregard the influence of the red cell size. We have studied this effect using an annular perfusion chamber according to Baumgartner, with human umbilical arteries and a steady flow system. Perfusions were performed with reconstituted blood consisting of the appropriate washed red cells, aspirin treated and 51Cr labelled human platelets and human plasma. Perfusions were at a calculated vessel wall shear rate of 800 sec-1 for 5 min at 37°C. Platelet adherence was measured by 51Cr counting and controlled by morphometry. Human, goat and rabbit red blood cells were utilized. Human red blood cells (mean cell volume 100 f1) increase platelet adherence sevenfold, as the hematocrit increases from 0 to 60%. Human erythrocyte ghosts had a similar effect. Goat erythrocytes (m.c.v. 25 f1) caused no increment in adherence in the same hematocrit range. Rabbit erythrocytes (m.c.v. 70 f1) caused an intermediate increase in adherence.These data indicate that the red cell size is of major importance for platelet adherence. They may be explained by postulating that red cell rotation is responsible for diffusivity.

scholarly journals Red blood cell size is important for adherence of blood platelets to artery subendothelium

Blood ◽  
1983 ◽  
Vol 62 (1) ◽  
pp. 214-217 ◽  
Author(s):  
PA Aarts ◽  
PA Bolhuis ◽  
KS Sakariassen ◽  
RM Heethaar ◽  
JJ Sixma
Keyword(s):  
Red Blood Cells ◽  
Cell Size ◽  
Blood Cells ◽  
Blood Platelets ◽  
Red Cells ◽  
Cell Diameter ◽  
Red Cell ◽  
Human Red Blood Cells ◽  
Platelet Adherence ◽  
Order Of Magnitude

Abstract The hematocrit is one of the main factors influencing platelet adherence to the vessel wall. Raising the hematocrit causes an increase of platelet accumulation of about an order of magnitude. Our studies concern the role of red cell size. We have studied this effect using an annular perfusion chamber, according to Baumgartner, with human umbilical arteries and a steady-flow system. Normal human red blood cells (MCV 95 cu mu) increased platelet adherence sevenfold, as the hematocrit increases from 0 to 0.6. Small erythrocytes from goats (MCV 25 cu mu) caused no increment in adherence in the same hematocrit range. Rabbit erythrocytes (MCV 70 cu mu) caused an intermediate increase in adherence. Red blood cells from newborns (MCV 110–130 cu mu) caused a larger increase in platelet adherence than normal red cells at hematocrit 0.4. These results were further confirmed with large red blood cells from two patients. Experiments with small red cells (MCV 70 cu mu) of patients with iron deficiency showed that platelet adherence was similar to normal red cells, provided the red cell diameter was normal. Small red blood cells of a patient with sideroblastic anemia caused decreased adherence. These data indicate that red cell size is of major importance for platelet adherence. Red cell diameter is more important than average volume. However, for size differences in the human range, the hematocrit remains the dominant parameter.

scholarly journals Red blood cell size is important for adherence of blood platelets to artery subendothelium

Blood ◽  
1983 ◽  
Vol 62 (1) ◽  
pp. 214-217 ◽  
Author(s):  
PA Aarts ◽  
PA Bolhuis ◽  
KS Sakariassen ◽  
RM Heethaar ◽  
JJ Sixma
Keyword(s):  
Red Blood Cells ◽  
Cell Size ◽  
Blood Cells ◽  
Blood Platelets ◽  
Red Cells ◽  
Cell Diameter ◽  
Red Cell ◽  
Human Red Blood Cells ◽  
Platelet Adherence ◽  
Order Of Magnitude

The hematocrit is one of the main factors influencing platelet adherence to the vessel wall. Raising the hematocrit causes an increase of platelet accumulation of about an order of magnitude. Our studies concern the role of red cell size. We have studied this effect using an annular perfusion chamber, according to Baumgartner, with human umbilical arteries and a steady-flow system. Normal human red blood cells (MCV 95 cu mu) increased platelet adherence sevenfold, as the hematocrit increases from 0 to 0.6. Small erythrocytes from goats (MCV 25 cu mu) caused no increment in adherence in the same hematocrit range. Rabbit erythrocytes (MCV 70 cu mu) caused an intermediate increase in adherence. Red blood cells from newborns (MCV 110–130 cu mu) caused a larger increase in platelet adherence than normal red cells at hematocrit 0.4. These results were further confirmed with large red blood cells from two patients. Experiments with small red cells (MCV 70 cu mu) of patients with iron deficiency showed that platelet adherence was similar to normal red cells, provided the red cell diameter was normal. Small red blood cells of a patient with sideroblastic anemia caused decreased adherence. These data indicate that red cell size is of major importance for platelet adherence. Red cell diameter is more important than average volume. However, for size differences in the human range, the hematocrit remains the dominant parameter.

scholarly journals STUDIES ON HEMAGGLUTINATION AND HEMOLYSIS BY ESCHERICHIA COLI ANTISERA

1952 ◽  
Vol 96 (1) ◽  
pp. 1-15 ◽  
Author(s):  
Erwin Neter ◽  
Lee F. Bertram ◽  
Dorothy A. Zak ◽  
Miriam R. Murdock ◽  
Carl E. Arbesman
Keyword(s):  
Escherichia Coli ◽  
Guinea Pig ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Homologous Blood ◽  
E Coli ◽  
Blood Group A ◽  
Human Red Blood Cells ◽  
Order Of Magnitude ◽  
Group A

A study on hemagglutination and hemolysis by Escherichia coli O111 and O55 (rabbit) antisera and on hemagglutination and hemolysis inhibition by E. coli O111 and O55 antigens revealed the following facts. 1. Red blood cells of man, dog, rabbit, guinea pig, sheep, rat, and chicken adsorb E. coli O111 and O55 antigens and thus become specifically agglutinable by the homologous E. coli antisera. 2. The adsorption of these E. coli antigens is a function of the concentration of the antigen, the time (from 5 minutes to 2 hours) of treatment of the red blood cells with the antigen, and the concentration of the red blood cells used. 3. Red blood cells of man and sheep adsorb simultaneously both antigens, as indicated by the fact that both antisera give agglutination of all red blood cells. Complete agglutination does not occur when a mixture of red blood cells treated separately with the two antigens is added to one or the other of the two antisera. 4. Treatment of red blood cells of man with one of the antigens does not block the adsorption of the second antigen. Human cells treated with either or both antigens are still agglutinated by the homologous blood group (A, B, and Rh)-specific antibodies. 5. In the presence of guinea pig complement, E. coli O111 and O55 antisera produce hemolysis of modified human red blood cells in titers of the same order of magnitude as those giving hemagglutination and bacterial agglutination. The same antisera produce hemolysis of sheep cells treated with the identical antigens in titers exceeding by far those giving agglutination of modified human or sheep red blood cells. 6. Both sediment and supernate of a boiled E. coli suspension are capable of modifying red blood cells for E. coli hemagglutination; in contrast, the supernate obtained from an unboiled suspension and then heated does not modify red blood cells for hemagglutination, although it contains the antigen which can specifically adsorb E. coli antibodies, as shown by means of the hemagglutination and hemolysis inhibition tests. 7. Both the unheated and the boiled suspensions of E. coli O111 and O55 inhibit hemagglutination and hemolysis specifically. 8. Rabbit red blood cells modified by either E. coli O111 or 055 antigens, upon intravenous injection into rabbits, engender specific E. coli antibodies. The significance of the results is discussed.

scholarly journals Voltage dependence of DIDS-insensitive chloride conductance in human red blood cells treated with valinomycin or gramicidin.

1994 ◽  
Vol 104 (5) ◽  
pp. 961-983 ◽  
Author(s):  
J C Freedman ◽  
T S Novak ◽  
J D Bisognano ◽  
P R Pratap
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Disulfonic Acid ◽  
Mean Cell Volume ◽  
Partial Inhibition ◽  
Human Red Blood Cells ◽  
Specific Effects ◽  
Voltage Curve ◽  
Current Voltage Curve ◽  
Cl Conductance

Net K and Cl effluxes induced by valinomycin or by gramicidin have been determined directly at varied external K, denoted by [K]o, in the presence and absence of the anion transport inhibitors DIDS (4,4'-diiso-thiocyano-2,2'-disulfonic acid stilbene), and its less potent analogue SITS (4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid). The results confirm that pretreatment with 10 microM DIDS, or 100 microM SITS, for 30 min at 23 degrees C inhibits conductive Cl efflux, measured in the continued presence of the inhibitors at 1 mM [K]o, by only 59-67%. This partial inhibition by 10 microM DIDS at 1 mM [K]o remains constant when the concentration of DIDS, or when the temperature or pH during pretreatment with DIDS, are increased. Observations of such partial inhibition previously prompted the postulation of two Cl conductance pathways in human red blood cells: a DIDS-sensitive pathway mediated by capnophorin (band 3 protein), and a DIDS-insensitive pathway. The present experiments demonstrate that at [K]o corresponding to values of EK between -35 and 0 mV the DIDS-insensitive component of net Cl efflux is negligible, being < or = 0.1 muMol/g Hb/min, both with valinomycin (1 microM) and with gramicidin (0.06 microgram/ml). At lower [K]o, where EK is below approximately -35 mV, the DIDS-insensitive fraction of net Cl efflux increases to 2.6 muMol/g Hb/min with valinomycin (1 microM), and to 4.8 muMol/g Hb/min with gramicidin (0.06 microgram/ml). With net fluxes determined from changes in mean cell volume, and with membrane potentials measured from changes in the external pH of unbuffered red cell suspensions, a current-voltage curve for DIDS-insensitive Cl conductance has been deduced. While specific effects of varied [K]o on net Cl efflux are unlikely but cannot strictly be ruled out, the results are consistent with the hypothesis that DIDS-insensitive Cl conductance turns on at an Em of approximately -40 mV.

scholarly journals How Do Red Blood Cells Die?

2021 ◽  
Vol 12 ◽  
Author(s):  
Perumal Thiagarajan ◽  
Charles J. Parker ◽  
Josef T. Prchal
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Red Cells ◽  
Cell Labeling ◽  
Red Cell ◽  
Average Life Span ◽  
Human Red Blood Cells ◽  
Physicochemical Changes ◽  
Cell Clearance

Normal human red blood cells have an average life span of about 120 days in the circulation after which they are engulfed by macrophages. This is an extremely efficient process as macrophages phagocytose about 5 million erythrocytes every second without any significant release of hemoglobin in the circulation. Despite large number of investigations, the precise molecular mechanism by which macrophages recognize senescent red blood cells for clearance remains elusive. Red cells undergo several physicochemical changes as they age in the circulation. Several of these changes have been proposed as a recognition tag for macrophages. Most prevalent hypotheses for red cell clearance mechanism(s) are expression of neoantigens on red cell surface, exposure phosphatidylserine and decreased deformability. While there is some correlation between these changes with aging their causal role for red cell clearance has not been established. Despite plethora of investigations, we still have incomplete understanding of the molecular details of red cell clearance. In this review, we have reviewed the recent data on clearance of senescent red cells. We anticipate recent progresses in in vivo red cell labeling and the explosion of modern proteomic techniques will, in near future, facilitate our understanding of red cell senescence and their destruction.

scholarly journals Ionic and osmotic equilibria of human red blood cells treated with nystatin.

1979 ◽  
Vol 74 (2) ◽  
pp. 157-185 ◽  
Author(s):  
J C Freedman ◽  
J F Hoffman
Keyword(s):  
Red Blood Cells ◽  
Cell Volume ◽  
Blood Cells ◽  
Osmotic Coefficients ◽  
Virial Equation ◽  
Red Cell ◽  
Extracellular Solution ◽  
Red Cell Volume ◽  
Human Red Blood Cells ◽  
Cell Volumes

Human red blood cells have been incubated in the presence of nystatin, which allows Na and K, as well as Cl and pH to equilibrate rapidly when cell volume is set with external impermeant sucrose. The intracellular mean ionic activity coefficients, relative to values in the extracellular solution, for KCl and NaCl are 1.01 +/- 0.02 and 0.99 +/- 0.02 (SD, n = 10), respectively, and are independent of external pH, pH o, and of [sucrose]o. With nystatin the dependence of red cell volume on [sucrose]o deviates from ideal osmotic behavior by as much as a factor of three. A virial equation for the osmotic coefficient, phi, of human hemoglobin, Hb, accounts for the cell volumes, and is the same as that which describes Adair's measurements of phi Hb for Hb isolated from sheep and ox bloods. In the presence of nystatin the slope of the acid-base titration curve of the cells is independent of cell volume, implying that the charge on impermeant cellular solutes is independent of Hb concentration at constant pH. By modifying the Jacobs-stewart equations (1947. J. Cell. Comp. Physiol. 30: 79--103) with the osmotic coefficients of Hb and of salts, a nonideal thermodynamic model has been devised which predicts equilibrium Donnan ratios and red cell volume from the composition of the extracellular solution and from certain parameters of the cells. In addition to accounting for the dependence of cell volume on osmotic pressure, the model also describes accurately the dependence of Donnan ratios and cell volumes on pHo either in the presence or absence of nystatin.

Utilization of Ion Beam Etching in Conjunction With Scanning Electron Microscopy to Study Red Blood Cell Structure

1973 ◽  
Vol 31 ◽  
pp. 446-447
Author(s):  
M. Spector ◽  
L. C. Burns ◽  
S. L. Kimzey
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Ion Beam ◽  
Cell Structure ◽  
Etching Time ◽  
Red Cell ◽  
Ion Beam Etching ◽  
Human Red Blood Cells ◽  
Argon Ion ◽  
Scanning Electron

Human red blood cells (Fig. 1) were ion beam etched in the specimen chamber of a scanning electron microscope in order to study the red cell structure. The red blood cells were fixed in glutaraldehyde and critical point dried in carbon dioxide prior to etching. Etching was carried out at about 10−4 torr using 3KV through 20KV argon ion beams at angles of incidence of 10, 38, and 90 degrees. In some cases the red cells were rotated at about 2 rotations per minute in the ion beam. Etching time varied from 1 to 30 minutes. After etching, the cells were removed from the microscope and coated with carbon and gold palladium before being reinserted in the microscope for examination.

Preferential localisation of red cell vacuoles to pathologically shaped human red blood cells

2009 ◽  
Vol 43 (1) ◽  
pp. 41-44
Author(s):  
Judith Demeter ◽  
Zoltan Magyar ◽  
Fatima Varga ◽  
Miklós Szathmári ◽  
Dezsö Lehoczky ◽  
...  
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Red Cell ◽  
Human Red Blood Cells
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