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      Hemodialysis Neutropenia Correlates with a Decreased Filterability and an Increase in the Number of Cytoplasmic Actin Filaments in Peripheral Blood Neutrophils, Which Is Preceded by a Decrease in the Number of Surface Expression of L-Selectin

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          In order to clarify the precise cellular mechanism of hemodialysis neutropenia, we examined the changes in the viscoelasticity of peripheral blood neutrophils using both the micropore and the microchannel filtration methods, and the changes in the neutrophil surface expression of Mac-1, L-selectin and sialyl Lewis X and the cytoplasmic expression of the actin filaments using a flow cytometric analysis during a dialysis session. Five patients with chronic renal failure were selected who showed a nadir leukocyte count in peripheral blood at 30 min after the initiation of the dialysis session. The neutrophil count also reached a nadir at 30 min and thereafter returned to almost the predialysis level by 180 min. Both the micropore filtration time and the microchannel passage time, which reflect the viscoelasticity of the peripheral blood neutrophils, correlated inversely with the neutrophil count. At the nadir of neutropenia, the neutrophils were observed to have become both adhesive and viscoelastic. The actin filaments in the neutrophil cytoplasm gradually increased in number from the start of dialysis, reaching a peak level at 30 min, and thereafter decreasing to predialysis levels. The Mac-1 expression continuously increased up from 30 min until the end of dialysis. The L-selectin expression first decreased at 15 min, but thereafter returned to predialysis levels within 60 min. The SLe<sup>x</sup> expression did not change throughout the course of the session. These results thus indicated the neutrophil counts during a dialysis session to inversely correlate with the viscoelasticity of the neutrophils expressed by the micropore filtration time or microchannel passage time, which possibly depends on the contents of cytoplasmic actin filaments. In addition, the shedding of L-selectin from neutrophil surface may also be involved in the first step of hemodialysis neutropenia.

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          Most cited references 5

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          Integrins: a family of cell surface receptors.

           Thomas Hynes (1987)
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            Modified cell-flow microchannels in a single-crystal silicon substrate and flow behavior of blood cells.

            Previously reported cell-flow microchannels in a single-crystal silicon substrate (Microvasc. Res. 44, 226-240, 1992) have been modified, and flow behavior of blood cells is described using flow rate-time curves and video pictures. The principal structure (2600 identically sized channels in parallel) was retained to give the same simple quantitative measure of the total flow rate for blood cell suspensions under constant suction. Level areas (terraces) were placed at the entrance and exit sides of the parallel channels level with the channel depth (4.5 microns) so that blood cells just entering into and flowing out of the channels could be more clearly observed under reflecting illumination. Three lengths (10, 20, and 100 microns) of channel were used each with a terrace width of 30 microns. In agreement with calculated values, the resistance to flow at the terrace portion was shown to be nearly equal to that per 10 microns of the channel portion. Clearer pictures were obtained of channel blocking by activated leukocytes and platelet aggregates after addition of each stimulant. Erythrocyte aggregates showed easy transit even through the 100-microns-long channels and through narrow spaces, including gaps probably narrower than 2 microns, which were formed between plugging leukocytes at the terrace portion.
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              Leucocyte-endothelial interactions and regulation of leucocyte migration


                Author and article information

                S. Karger AG
                July 1999
                21 June 1999
                : 82
                : 3
                : 214-220
                Departments of aDermatology and bInternal Medicine, Institute of Clinical Medicine, University of Tsukuba, Ibaraki, Japan
                45405 Nephron 1999;82:214–220
                © 1999 S. Karger AG, Basel

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                Figures: 7, Tables: 1, References: 25, Pages: 7
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