scholarly journals On the relationship between hæmolysis and the phagocytosis of red blood cells

1989 ◽  
Vol 257 (1) ◽  
pp. C114-C121 ◽  
Author(s):  
N. al-Rohil ◽  
M. L. Jennings

In this study the volume-dependent or N-ethylmaleimide (NEM)-stimulated, ouabain-insensitive K+ influx and efflux were measured with the tracer 86Rb+ in rabbit red blood cells. The purpose of the work was to examine the rabbit as a potential model for cell volume regulation in human SS red blood cells and also to investigate the relationship between the NEM-reactive sulfhydryl group(s) and the signal by which cell swelling activates the transport. Ouabain-resistant K+ efflux and influx increase nearly threefold in cells swollen hypotonically by 15%. Pretreatment with 2 mM NEM stimulates efflux 5-fold and influx 10-fold (each measured in an isotonic medium). The ouabain-resistant K+ efflux was dependent on the major anion in the medium. The anion dependence of K+ efflux in swollen or NEM-stimulated cells was as follows: Br- greater than Cl- much greater than NO3- = acetate. The magnitudes of both the swelling- and the NEM-stimulated fluxes are much higher in young cells (density separated but excluding reticulocytes) than in older cells. Swelling- or NEM-stimulated K+ efflux in rabbit red blood cells was inhibited 50% by 1 mM furosemide, and the inhibitory potency of furosemide was enhanced by extracellular K+, as is known to be true for human AA and low-K+ sheep red blood cells. The swelling-stimulated flux in both rabbit and human SS cells has a pH optimum at approximately 7.4. We conclude that rabbit red blood cells are a good model for swelling-stimulated K+ transport in human SS cells.(ABSTRACT TRUNCATED AT 250 WORDS)


2009 ◽  
Vol 5 (2) ◽  
pp. 95-104 ◽  
Author(s):  
B. A. Rasmusen ◽  
Elizabeth M. Tucker ◽  
J. C. Ellory ◽  
R. L. Spooner

2008 ◽  
Vol 11 (3) ◽  
pp. 433-437 ◽  
Author(s):  
M. Pourjafar ◽  
G.H.A. Kojouri ◽  
A. Jafari Dehkordi ◽  
S. Sharifi ◽  
T. Esmaeili

1994 ◽  
Vol 193 (1) ◽  
pp. 183-190 ◽  
Author(s):  
J Pesquero ◽  
T Roig ◽  
J Bermudez ◽  
J Sanchez

The present study investigates energy metabolism by trout red blood cells. It is shown that they are able to use pyruvate at physiological concentrations as an aerobic source of energy. Moreover, microcalorimetric data suggest that trout erythrocytes are also able to use internal substrates, at least when maintained in vitro. Although the actual nature of these substrates has not been elucidated, glycogen appears to be the most probable. The relationship between heat dissipation and oxygen consumption suggests that most of the oxygen is used to oxidize substrates, and the inhibition of respiratory activity by antimycin A indicates that there is no substantial utilisation of non-respiratory oxygen. However, the oxygen uptake by these cells does not appear to be related to substrate utilisation, measured from transformation of labelled molecules (either pyruvate or glucose); this may be due to mixing of labelled compounds with non-labelled molecules in the intracellular pools, because of the low metabolic rate of these cells.


1997 ◽  
Vol 272 (4) ◽  
pp. C1099-C1111 ◽  
Author(s):  
M. Berenbrink ◽  
Y. R. Weaver ◽  
A. R. Cossins

The volume sensitivity of different K flux pathways has been determined in trout red blood cells subjected to volume perturbation. Gentle hyposmotic swelling induced a K influx in a Cl-containing saline but not in NO3- or methanesulfonate (MeSF)-containing salines, consistent with the activation of a Cl-dependent flux. Extreme hyposmotic swelling led to larger K fluxes in all salines but with reduced anion discrimination of the Cl-dependent flux. In contrast to these graded responses, isosmotic swelling using ammonium chloride or beta-adrenergic stimulation activated only Cl-dependent fluxes in an all-or-none fashion. The relationship between the hyposmotically and isosmotically induced pathways was studied by coactivation using either ammonium chloride or isoproterenol with anisosmotic treatment. Cells in ammonium chloride-containing hyposmotic salines showed no additive K flux over that induced by hyposmotic treatment alone, indicating that the isosmotically induced Cl-dependent flux was identical to the hyposmotically induced Cl-dependent flux. However, cells coactivated by hyposmotic and beta-adrenergic treatment showed a small Cl-dependent flux in addition to that induced by hyposmotic treatment alone. This small third component was unaffected by anisosmotic treatment. We conclude that the major Cl-dependent and Cl-independent K flux pathways are distinct and separate and that the former has an anion dependence that varies with cell volume and a volume sensitivity that varies with ionic strength.


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