The rheological properties of normal erythrocytes appear to be determined largely by those of the red cell membrane. In sickle cell disease, the intracellular polymerization of sickle hemoglobin upon deoxygenation leads to a marked increase in intracellular viscosity and elastic stiffness, and also has indirect effects on the cell membrane. In order to estimate the components of abnormal cell rheology due to the polymerization process (and that due to the membrane abnormalities), we have developed a mathematical model of whole cell deformability in narrow vessels. This model uses hydrodynamic lubrication theory to describe the pulsatile flow in the gap between a cell and the vessel wall. We use published values of normal and sickle cell membrane elastic modulus and of sickle hemoglobin viscous and elastic moduli as a function of oxygen saturation to estimate the cell deformation and relative hydrodynamic resistance as a function of oxygen saturation for sickle erythrocytes. The model should be useful for reconciling the vast and disparate sets of data available on the abnormal properties of sickle cell hemoglobin and sickle erythrocyte membranes--the two main factors that lead to pathology in patients with this disease.

Agency
National Institute of Health (NIH)
Institute
National Center for Research Resources (NCRR)
Type
Intramural Research (Z01)
Project #
1Z01RR010361-04
Application #
3767457
Study Section
Project Start
Project End
Budget Start
Budget End
Support Year
4
Fiscal Year
1994
Total Cost
Indirect Cost
Name
National Center for Research Resources
Department
Type
DUNS #
City
State
Country
United States
Zip Code