Red cell aggregation in blood flow

1976 ◽  
Vol 54 (4) ◽  
pp. 159-167 ◽  
Author(s):  
H. Schmid-Sch�nbein ◽  
G. Gallasch ◽  
J. Gosen ◽  
E. Volger ◽  
H. J. Klose
1976 ◽  
Vol 54 (4) ◽  
pp. 149-157 ◽  
Author(s):  
H. Schmid-Sch�nbein ◽  
G. Gallasch ◽  
J. Gosen ◽  
E. Volger ◽  
H. J. Klose

1996 ◽  
Vol 49 (5) ◽  
pp. 1268-1275 ◽  
Author(s):  
Per Liss ◽  
Anders Nygren ◽  
Ulf Olsson ◽  
Hans R. Ulfendahl ◽  
Uno Erikson

Radiology ◽  
1983 ◽  
Vol 148 (3) ◽  
pp. 799-802 ◽  
Author(s):  
B Sigel ◽  
J Machi ◽  
J C Beitler ◽  
J R Justin

1989 ◽  
Vol 256 (3) ◽  
pp. H898-H905 ◽  
Author(s):  
R. Y. Chen ◽  
R. D. Carlin ◽  
S. Simchon ◽  
K. M. Jan ◽  
S. Chien

In 10 pentobarbitalized dogs, plasma viscosity (Ep) was raised fourfold while apparent blood viscosity (Ea) increased about twofold by two steps of exchange transfusion of 200 ml of plasma with plasma containing high molecular weight dextran (mol wt 500,000, 20% wt/vol). Elevation of Ea was primarily caused by an increase of Ep but not red cell aggregation. As Ea increased, regional blood flow (by 15-microns microspheres) remained constant in most organs but reduced in the small intestine, spleen, and thyroid gland. Vascular hindrance (Z), which reflects the state of vascular geometry, was calculated as flow resistance per Ea. Among various organs, a reduction in Z was noted in the heart, liver, pancreas, kidney, brain, and adrenal gland. In myocardium, there was a progressive reduction of the endocardial-to-epicardial flow ratio, indicating a less profound vasodilation in endocardium than epicardium. These results indicate that dextran-induced hyperviscosity leads to a compensatory vasodilation in several vital organs thus serving to maintain blood flow and nutrient transport.


1971 ◽  
Vol 3 (6) ◽  
pp. 428-435 ◽  
Author(s):  
P.M. Scholz ◽  
J. Engeset ◽  
N.A. Matheson ◽  
U.F. Gruber

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