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The Effect of Hemofiltration on Fiber Platelet Concentration
Author(s) -
Drake Kenneth L.,
Eckstein Eugene C.
Publication year - 1981
Publication title -
artificial organs
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.684
H-Index - 76
eISSN - 1525-1594
pISSN - 0160-564X
DOI - 10.1111/j.1525-1594.1981.tb04018.x
Subject(s) - platelet , concentration polarization , fiber , volumetric flow rate , chemistry , shear rate , inlet , materials science , chromatography , platelet adhesion , composite material , analytical chemistry (journal) , membrane , adhesion , mechanics , rheology , medicine , biochemistry , mechanical engineering , physics , engineering
Experimental methods and apparatus were developed to measure platelet concentration in an ultrafiltering hollow fiber with blood and ultrafiltrative flow rates that are characteristic of current hemofiltration practice. Values are presented for the adjusted local platelet concentration, which allows for the expected increase due to loss of ultrafiltrate volume. Platelet concentrations in fiber samples are of interest since ultrafiltration can create platelet polarization in a fashion similar to the concentration polarization that occurs for proteins. For many combinations of inlet flow rate, ultrafiltrative flow rate, and fiber dimension, there are significant elevations in adjusted fiber platelet concentration. The adjusted platelet concentrations of the outflow samples are nominally equal to those of the feed (reservoir) samples; thus, reaction and adhesion of platelets is not a significant source of fiber concentration. Experiments with fibers of different diameters indicate that, as expected in concentration polarization, the excess platelets are located near the wall. Data for the fiber platelet concentration depend in a complex fashion upon the inlet wall shear rate and ultrafiltrative velocity. For certain fixed ultrafiltrative velocities, a maximum fiber platelet concentration occurs at an intermediate inlet wall shear rate. The data are qualitatively explained by an extension of a published model involving diffusive, ultrafiltrative, and wall‐induced fluxes of red cells and platelets.