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RE Samuel, AE Guzman and RW Briehl
Department of Physiology and Biophysics, Albert Einstein College of
Medicine, Bronx, NY 10461.
The kinetics of hemoglobin S gelation are critical in sickle disease
because microvascular obstruction can be avoided if red blood cells pass
these vessels during the delay time, before polymerization and gelation
occur in sufficient degree to rigidify the cells. Kinetics, including the
delay time and the closely related exponential progress rate, are highly
sensitive to hemoglobin concentration and degree of deoxygenation. Kinetics
are also greatly accelerated by shear, an effect that may contribute to
pathogenesis, since red blood cells deform and can undergo shear in vivo.
Here we examine the joint dependence of kinetics on shear and hemoglobin
concentration. As shear rate increases, the concentration dependence of the
exponential progress rate decreases. The large decrease in concentration
dependence supports the conclusion that acceleration of gelation by shear
is due to breakage and not to enhancement of heterogeneous nucleation.
Under shear, new fibers are created by breakage of existing ones, as well
as by heterogeneous nucleation. At high shear, the rate of new fiber
creation by breakage is very great and dominates that by heterogeneous
nucleation. Therefore, if breakage depended only on shear rate and were
independent of the concentration of hemoglobin in solution, the
concentration dependence of kinetics should vanish. Although it decreases,
it does not disappear. The concentration dependence that remains at high
shear arises from (1) the direct contribution of fiber growth rate to the
exponential progress rate, (2) the dependence of breakage rate on fiber
growth rate, and (3) the dependence of solution viscosity on hemoglobin
concentration.
This article has been cited by other articles:
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| Copyright © 1993 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||
