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Region Hovedstaden - en del af Københavns Universitetshospital
Udgivet

Red blood cell sodium transport in patients with cirrhosis

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DOI

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Vis graf over relationer
Patients with advanced cirrhosis have abnormal sodium homoeostasis. The study
was undertaken to quantify the sodium transport across the plasma membrane of
red blood cells (RBC) in patients with cirrhosis. RBC efflux and influx of sodium
were studied in vitro with tracer 22Na+ according to linear kinetics in 24 patients
with cirrhosis and 14 healthy controls. The sodium efflux was modified by ouabain
(O), furosemide (F) and a combination of O and F (O + F). RBC sodium
was significantly decreased (46 versus control 63 mmol l1, P<0001) and
directly related to serum sodium (r = 057, P<005). The RBC fractional sodium
efflux was higher in patients with cirrhosis (+46%, P<001) compared to controls.
Inhibition in both high (145 mmol l1)- and low (120 mmol l1)-sodium
buffers showed that the F-insensitive sodium efflux was twice as high in cirrhosis
as in controls (P = 003–0007), especially the O-sensitive, F-insensitive efflux
was increased (+ 225%, P = 001–0006). Fractional F-sensitive transport was
normal in cirrhosis. RBC sodium influx was largely normal in cirrhosis. In conclusion,
RBC sodium content is reduced in patients with cirrhosis with a direct relation
to serum sodium. Increased RBC sodium efflux is especially related to
ouabain-sensitive, furosemide-insensitive transport and thus most likely due to
upregulated activity of the sodium–potassium pump. The study gives no evidence
to an altered intracellular/extracellular sodium ratio or to a reduced fractional
furosemide-sensitive sodium transport in cirrhosis.
OriginalsprogEngelsk
TidsskriftClinical Physiology and Functional Imaging
Vol/bind36
Udgave nummer5
Sider (fra-til)359-367
Antal sider9
ISSN1475-0961
DOI
StatusUdgivet - sep. 2016

ID: 45445578