TY - JOUR
T1 - In vivo measurements of "apparent viscosity" and microvessel hematocrit in the mesentery of the cat
AU - Lipowsky, Herbert H.
AU - Usami, Shunichi
AU - Chien, Shu
N1 - Funding Information:
I Supported by USPHS
Copyright:
Copyright 2014 Elsevier B.V., All rights reserved.
PY - 1980/5
Y1 - 1980/5
N2 - The arteriovenous (A-V) distribution of microvessel hematocrit (Hmicro) was determined throughout successive microvascular divisions in cat mesentery from in vivo measurements of optical density. In vitro correlations of optical density and tube hematocrit in small-bore glass tubes permitted the computation of in vivo values of Hmicro for luminal diameters ranging from 20 to 70 μm. For smaller-size vessels, Hmicro was determined by microocclusion and red cell counting. The results demonstrate a monotonic fall in the ratio of Hmicro Hsystemic from 0.80 in the 70-μm arterioles to a minimum of 0.21 in the immediate postcapillaries (10 μm diameter) followed by a subsequent monotonic rise to 0.95 in the 70-μm venules. Conservation of red cell flux throughout the mesenteric network was partially demonstrated upon applying previously established in vitro relationships between discharge and tube hematocrits, the resulting disparity being attributed to the rheological behavior of blood and possible A-V shunting of red cells. Simultaneous measurements of pressure drop and red cell velocity in unbranched arterioles during systemic hemodilution facilitated a comparison of in vivo and in vitro (cone-plate viscometer) apparent viscosities (η). No significant differences between the two approaches were found for arteriole diameters ranging from 24 to 47 μm in the absence of leukocyte-endothelium adhesion, with 0 < Hmicro < 36% and vivo wall shear rates above 500 sec-1. In situ measurements of η were found to increase 74% due to leukocyte adhesion during sustained flow reductions, in one illustrative case. Values of η computed from the A-V distribution of Hmicro and the regression of η vs Hmicro (established without leukocyte adhesion), in comparison with previous measurements of the A-V distribution of η with leukocyte adhesion present, suggest that leukocyte adhesion may result in overall increases in η ranging from 100 to 200%, throughout the mesenteric network.
AB - The arteriovenous (A-V) distribution of microvessel hematocrit (Hmicro) was determined throughout successive microvascular divisions in cat mesentery from in vivo measurements of optical density. In vitro correlations of optical density and tube hematocrit in small-bore glass tubes permitted the computation of in vivo values of Hmicro for luminal diameters ranging from 20 to 70 μm. For smaller-size vessels, Hmicro was determined by microocclusion and red cell counting. The results demonstrate a monotonic fall in the ratio of Hmicro Hsystemic from 0.80 in the 70-μm arterioles to a minimum of 0.21 in the immediate postcapillaries (10 μm diameter) followed by a subsequent monotonic rise to 0.95 in the 70-μm venules. Conservation of red cell flux throughout the mesenteric network was partially demonstrated upon applying previously established in vitro relationships between discharge and tube hematocrits, the resulting disparity being attributed to the rheological behavior of blood and possible A-V shunting of red cells. Simultaneous measurements of pressure drop and red cell velocity in unbranched arterioles during systemic hemodilution facilitated a comparison of in vivo and in vitro (cone-plate viscometer) apparent viscosities (η). No significant differences between the two approaches were found for arteriole diameters ranging from 24 to 47 μm in the absence of leukocyte-endothelium adhesion, with 0 < Hmicro < 36% and vivo wall shear rates above 500 sec-1. In situ measurements of η were found to increase 74% due to leukocyte adhesion during sustained flow reductions, in one illustrative case. Values of η computed from the A-V distribution of Hmicro and the regression of η vs Hmicro (established without leukocyte adhesion), in comparison with previous measurements of the A-V distribution of η with leukocyte adhesion present, suggest that leukocyte adhesion may result in overall increases in η ranging from 100 to 200%, throughout the mesenteric network.
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U2 - 10.1016/0026-2862(80)90050-3
DO - 10.1016/0026-2862(80)90050-3
M3 - Article
C2 - 7382851
AN - SCOPUS:0018976258
SN - 0026-2862
VL - 19
SP - 297
EP - 319
JO - Microvascular Research
JF - Microvascular Research
IS - 3
ER -