Fahraeus-effect-reversal (FER) in compaction stasis (CS): microrheological and haemodynamic consequences of intravascular sedimentation of red cell aggregates.
Red cell aggregate sedimentation under gravitation produces pronounced and rapid "phase separation effects" culminating in "compaction stasis" (CS), i.e. almost complete stuffing of microvessels by RBC. This can be readily observed and monitored in microvessels of vertically placed mesentery preparations by a horizontally aimed intravital microscope as shown by (GOBEL et al. VIRCHOW's Arch., 1988,). "Layered flow", floatational plasma skimming and progressive increase in local tube hematocrit (HT) up to 100% ("compaction stasis") occurs during induced low flow states in vivo (here preferentially in postcapillary venules), as well as in vitro (non-permeable artificial micro tube networks). Quantitative densitometry and velocimetry in vertically placed microvessels demonstrates that the process of RCA sedimentation results in progressive vertical skewing of the velocity profile, culminating in standstill of the RBC-sediment in the dependent vessel half, with superfluent plasma and small aggregates in the upper vessel half. The theory of compaction stasis is developed: in striking contrast to the situation under high shear conditions, red cells travel on slower trajectories than plasma: due to "red cell undervelocity" the average residence times of RBC in a venule is much higher than that of plasma. Consequently, CS can be explained as the result of a FAHRAEUS effect reversal since the principle of mass conservation requires that HT much greater than HD. Network aspects and hemodynamic consequences are also incorporated into the theory.
Schmid-Schönbein
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Department of Physiology, RWTH-Klinikum, Aachen, FRG.
D000818:Animals; D001799:Blood Sedimentation; D004903:Erythrocyte Aggregation; D006439:Hemodynamics; D006487:Hemostasis; D008833:Microcirculation; D008955:Models, Cardiovascular; D012212:Rheology