Effect of erythrocyte aggregation on velocity profiles in venules
1 Department of Bioengineering University of California, San Diego, La Jolla, California 92093; and 2 Department of Biomedical Engineering, Johns Hopkins University, Baltimore, Maryland 21205 A recent whole organ study in cat skeletal muscle showed that the increase in venous resistance seen at re...
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Veröffentlicht in: | American journal of physiology. Heart and circulatory physiology 2001-01, Vol.280 (1), p.H222-H236 |
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Sprache: | eng |
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Zusammenfassung: | 1 Department of Bioengineering University of California, San
Diego, La Jolla, California 92093; and 2 Department of
Biomedical Engineering, Johns Hopkins University, Baltimore, Maryland
21205
A recent whole organ study in cat skeletal muscle showed that
the increase in venous resistance seen at reduced arterial pressures is
nearly abolished when the muscle is perfused with a nonaggregating red
blood cell suspension. To explore a possible underlying mechanism, we
tested the hypothesis that red blood cell aggregation alters flow
patterns in vivo and leads to blunted red blood cell velocity profiles
at reduced shear rates. With the use of fluorescently labeled red blood
cells in tracer quantities and a video system equipped with a gated
image intensifier, we obtained velocity profiles in venous microvessels
(45-75 µm) of rat spinotrapezius muscle at centerline velocities
between 0.3 and 14 mm/s (pseudoshear rates 3-120
s 1 ) under normal (nonaggregating) conditions and after
induction of red blood cell aggregation with Dextran 500. Profiles are
nearly parabolic (Poiseuille flow) over this flow rate range in the
absence of aggregation. When aggregation is present, profiles are
parabolic at high shear rates and become significantly blunted at
pseudoshear rates of 40 s 1 and below. These results
indicate a possible mechanism for increased venous resistance at
reduced flows.
venous resistance; blood constitutive equation; in vivo blood
viscosity; in vivo fluorescence microscopy; wall shear stress |
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ISSN: | 0363-6135 1522-1539 |
DOI: | 10.1152/ajpheart.2001.280.1.h222 |