Microrheology of erythrocytes, blood viscosity, and the distribution of blood flow in the microcirculation.

The normal rheological behavior of the red blood cells is prerequisite for the survival of the red cells and also for the functioning of microcirculation. Severe alterations of red cell deformability are incompatible with life. When compensated by anemia, even relatively severe rheological incompetence of individual red cells is tolerable. Functional loss of red cell deformability is widely known to occur under conditions of sustained hypoperfusion, and disseminated stagnation of blood in the paracapillary bed occurs. The resulting capillary occlusion does not necessarily reveal itself in grossly reduced flow rates or increased "total peripheral resistance," since it is compensated by shunting through microscopic anastomoses. The biological significance of the phenomenon of red cell aggregation (collateral loss of blood fluidity, "collateral blood viscidation") is related to hemodynamics only on the level of individual capillaries. Since the compensatory potentials of vasomotor factors at this level are also very high, the collateral viscidation is not only facilitated but by the same token partially compensated. Therefore, unless complicated by a defect in the macrocirculation, the biological significance of blood rheology seen under the aspects of entire organs is not primarily related to hemodynamics, but to diffusive transcapillary exchange. As a consequence of collateral blood viscidation, diffusion takes place under sub-optimal conditions. The available surface area for exchange is reduced, the diffusion distances are increased. In themselves, these changes are no acute threat to the survival of the entire individual. In combination with other defects, they are capable of sustaining prolonged states of flow arrest. Since the rheological properties of blood can be easily manipulated, sustained circulatory deficiencies can be avoided or treated by improving blood fluidity.