Permselectivity of the liver blood-lymph (ascitic fluid) barrier to macromolecules in decompensated cirrhosis: relation to calculated pore-size
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Permselectivity of the liver blood-lymph (ascitic fluid) barrier to macromolecules in decompensated cirrhosis: relation to calculated pore-size. / Henriksen, Jens Henrik Sahl.
I: Clinical physiology (Oxford, England), Bind 3, Nr. 2, 1983, s. 163-71.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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TY - JOUR
T1 - Permselectivity of the liver blood-lymph (ascitic fluid) barrier to macromolecules in decompensated cirrhosis: relation to calculated pore-size
AU - Henriksen, Jens Henrik Sahl
N1 - Keywords: Adult; Albumins; Ascitic Fluid; Blood; Capillary Permeability; Female; Filtration; Humans; Immunoglobulin G; Immunoglobulin M; Liver; Liver Cirrhosis, Alcoholic; Macromolecular Substances; Male; Middle Aged; Serum Albumin
PY - 1983
Y1 - 1983
N2 - This study was undertaken to investigate permselectivity of the liver blood-lymph (ascitic fluid) barrier to endogeneous marcomolecules in patients with decompensated cirrhosis. Albumin (mol wt 69,000), immunoglobulin-G (mol wt 160,000) and immunoglobulin-M (mol wt 900,000) were determined in plasma and ascitic fluid from 13 cirrhotic patients. As previously substantiated in patients with cirrhosis, the ascitic fluid/plasma concentration ratio (R) of a protein is proportional to the transport rate from blood to lymph (ascitic fluid). Mean Ralb = 0.28 and RIgG = 0.29 were identical, but significantly higher than, RIgM = 0.18 (P less than 0.01). Ralb was directly correlated to RIgG (r = 0.97, P less than 0.001) and to RIgM (r = 0.78, P less than 0.005). Mean RIgG/Ralb = 1.03, which expresses the relative flux rates between IgG and albumin, was significantly above the ratio between the free diffusion coefficients (DIgG/Dalb = 0.64, P less than 0.01). Mean RIgM/Ralb = 0.61 was significantly above DIgM/Dalb = 0.39 (P less than 0.05) and significantly below unity (P less than 0.01). The results are best explained by filtration as the dominant mechanism of the liver blood-lymph (ascitic fluid) exchange of endogeneous macromolecules. A significant 'sieving' is present in this barrier to the largest macromolecule (IgM). Calculations of pore-size equivalent to the observed permselectivity of macromolecules suggest microvascular gaps (or channels) with an average radius about 300 A, i.e. in the lower end of the range of gaps in normal liver sinusoids (from 200 to 5000 A).
AB - This study was undertaken to investigate permselectivity of the liver blood-lymph (ascitic fluid) barrier to endogeneous marcomolecules in patients with decompensated cirrhosis. Albumin (mol wt 69,000), immunoglobulin-G (mol wt 160,000) and immunoglobulin-M (mol wt 900,000) were determined in plasma and ascitic fluid from 13 cirrhotic patients. As previously substantiated in patients with cirrhosis, the ascitic fluid/plasma concentration ratio (R) of a protein is proportional to the transport rate from blood to lymph (ascitic fluid). Mean Ralb = 0.28 and RIgG = 0.29 were identical, but significantly higher than, RIgM = 0.18 (P less than 0.01). Ralb was directly correlated to RIgG (r = 0.97, P less than 0.001) and to RIgM (r = 0.78, P less than 0.005). Mean RIgG/Ralb = 1.03, which expresses the relative flux rates between IgG and albumin, was significantly above the ratio between the free diffusion coefficients (DIgG/Dalb = 0.64, P less than 0.01). Mean RIgM/Ralb = 0.61 was significantly above DIgM/Dalb = 0.39 (P less than 0.05) and significantly below unity (P less than 0.01). The results are best explained by filtration as the dominant mechanism of the liver blood-lymph (ascitic fluid) exchange of endogeneous macromolecules. A significant 'sieving' is present in this barrier to the largest macromolecule (IgM). Calculations of pore-size equivalent to the observed permselectivity of macromolecules suggest microvascular gaps (or channels) with an average radius about 300 A, i.e. in the lower end of the range of gaps in normal liver sinusoids (from 200 to 5000 A).
M3 - Journal article
C2 - 6682737
VL - 3
SP - 163
EP - 171
JO - Clinical Physiology
JF - Clinical Physiology
SN - 0144-5979
IS - 2
ER -
ID: 19398040