Erythrocyte deformation in a microfluidic cross-slot channel

RSC Advances ◽  
2014 ◽  
Vol 4 (68) ◽  
pp. 36079 ◽  
Author(s):  
Yann Henon ◽  
Gregory J. Sheard ◽  
Andreas Fouras
1978 ◽  
Vol 35 (1) ◽  
pp. 823-827 ◽  
Author(s):  
O. N. Ovchinnikov ◽  
E. M. Smirnov

Blood ◽  
1987 ◽  
Vol 69 (3) ◽  
pp. 727-734 ◽  
Author(s):  
K Kon ◽  
N Maeda ◽  
T Shiga

The effect of shear force (depending on shear rate and viscosity of extracellular medium) and hematocrit of RBC suspension on RBC deformation was studied quantitatively using a cone-plate rheoscope with various kinds of cells, ie, partially hemolyzed (PH) cells, density-fractionated intact cells, and diamide-treated cells. The deformation index (DI) of ellipsoidally deformed cells was shown to be a function of beta gamma eta ex(eta ex/eta in)alpha, where gamma eta ex is applied shear stress, eta ex and eta in are external and internal viscosities, respectively, and alpha and beta are adjustable parameters related to the membrane viscoelastic properties. The increase of suspension viscosity at higher hematocrits (Hts) generally enhanced the ellipsoidal deformation of cells, in the same manner as increasing the suspending medium viscosity of a diluted cell suspension. The suppressing effect on cell deformation appeared above a certain Ht. When intact cells were mixed with glutaraldehyde-treated, hardened cells, the ellipsoidal deformation of intact cells was disturbed. The suppression of deformation probably occurred through disturbance of laminar flow-lines around intact cells.


2001 ◽  
Vol 281 (4) ◽  
pp. C1158-C1164 ◽  
Author(s):  
Randy S. Sprague ◽  
Mary L. Ellsworth ◽  
Alan H. Stephenson ◽  
Andrew J. Lonigro

Previously, we reported that red blood cells (RBCs) of rabbits and humans release ATP in response to mechanical deformation and that this release of ATP requires the activity of the cystic fibrosis transmembrane conductance regulator (CFTR). It was reported that cAMP, acting through a cAMP-dependent protein kinase, PKA, is an activator of CFTR. Here we investigate the hypothesis that cAMP stimulates ATP release from RBCs. Incubation of human and rabbit RBCs with the direct activator of adenylyl cyclase, forskolin (10 or 100 μM), with IBMX (100 μM), resulted in ATP release and increases in intracellular cAMP. In addition, epinephrine (1 μM), a receptor-mediated activator of adenylyl cyclase, stimulated ATP release from rabbit RBCs. Moreover, incubation of human and rabbit RBCs with an active cAMP analog [adenosine 3′5′-cyclic monophosphorothioate Sp-isomer (Sp-cAMP, 100 μM)] resulted in ATP release. In contrast, forskolin and Sp-cAMP were without effect on dog RBCs, cells known not to release ATP in response to deformation. When rabbit RBCs were incubated with the inactive cAMP analog and inhibitor of PKA activity, adenosine 3′,5′-cyclic monophosphorothioate Rp-isomer (100 μM), deformation-induced ATP release was attenuated. These results are consistent with the hypothesis that adenylyl cyclase and cAMP are components of a signal-transduction pathway relating RBC deformation to ATP release from human and rabbit RBCs.


Science ◽  
1974 ◽  
Vol 184 (4133) ◽  
pp. 165-166 ◽  
Author(s):  
D. W. Matheson ◽  
J. L. Howland

2000 ◽  
Author(s):  
Stanislav S. Bessmeltsev ◽  
Alexander V. Lendiaev ◽  
Yulia A. Skvortsova ◽  
Vladimir A. Tarlykov

1987 ◽  
Vol 52 (1) ◽  
pp. 58-63
Author(s):  
P. A. Novikov ◽  
L. Ya. Lyubin ◽  
V. I. Novikova

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