Evidence that cell surface charge reduction modifes capillary red cell velocity-flux relationships in hamster cremaster muscle.

1. From capillary red cell velocity (V)-flux (F) relationships of hamster cremaster muscle a yield velocity (VF = 0) can be derived at which red cell flux is zero. Red cell velocity becomes intermittent and/or red blood cells come to a complete standstill for velocities close to this yield velocity, and, at the same time, capillary tube haematocrit becomes very low. 2. We have tested whether the net negative charge of red blood cells (RBCs) contributes to the magnitude of VF = 0. Velocity-flux relationships were measured for normal cells, normal cells labelled with the fluorescent dye calcein (LRBCs), and red cells treated with hexadimethrine to mask negative charge and labelled with calcein as well (HDM-LRBCs). Measurements were done in a hamster cremaster muscle preparation applying video in vivo microscopy. 3. Hexadimethrine treatment reduced the net negative surface charge of red cells to 20% of control as estimated from transmission electron microscopy using a ferritin tagging technique. The values of VF = 0 found for normal red cells and HDM-LRBCs were 86 +/- 15 and 31 +/- 17 microns s-1, +/- S.E.M., n = 12, respectively, which were significantly different (P < 0.05). For normal cells and cells labelled with calcein only, VF = 0 values were 63 +/- 14 and 65 +/- 13 microns s-1, n = 8, respectively, which were not significantly different. The effect of HDM treatment did not alter filterability of the red cells as estimated from transit times through 5 microns pores. 4. The present findings demonstrate that the net negative charge of RBCs contributes significantly to the yield velocity for red blood cells entering capillaries and flowing through them. HDM treatment reduced the net negative charge of red blood cells and may have caused cells to enter capillaries more easily owing to reduced electrostatic repulsion at the capillary entrance. In addition, HDM treatment may have lowered intracapillary flow resistance by a reduction in electrostatic repulsive forces between red blood cells and negatively charged (macromolecules on) capillary endothelial cells at sites of irregular capillary cross-sectional shape, without significantly affecting the lubricating properties of the capillary endothelial glycocalyx and/or associated plasma macromolecules.