title: Red blood cell sodium transport in patients with cirrhosis.
abstract: 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 (22) Na(+) 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 (4·6 versus control 6·3 mmol l(-1) , P<0·001) and directly related to serum sodium (r = 0·57, P<0·05). The RBC fractional sodium efflux was higher in patients with cirrhosis (+46%, P<0·01) compared to controls. Inhibition in both high (145 mmol l(-1) )- and low (120 mmol l(-1) )-sodium buffers showed that the F-insensitive sodium efflux was twice as high in cirrhosis as in controls (P = 0·03-0·007), especially the O-sensitive, F-insensitive efflux was increased (+ 225%, P = 0·01-0·006). 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.
authors.affiliation: Department of Clinical Physiology 239, Center for Functional and Diagnostic Imaging and Research, University of Copenhagen, Copenhagen, Denmark.
authors.forename: Ulrik Lütken
authors.initials: UL
authors.lastname: Henriksen
authors.affiliation: Gastrounit Medical Division, Hvidovre Hospital, Faculty of Medicine and Health Sciences, University of Copenhagen, Copenhagen, Denmark.
authors.forename: Marianne
authors.initials: M
authors.lastname: Kiszka-Kanowitz
authors.affiliation: Gastrounit Medical Division, Hvidovre Hospital, Faculty of Medicine and Health Sciences, University of Copenhagen, Copenhagen, Denmark.
authors.forename: Flemming
authors.initials: F
authors.lastname: Bendtsen
authors.affiliation: Department of Clinical Physiology 239, Center for Functional and Diagnostic Imaging and Research, University of Copenhagen, Copenhagen, Denmark.
authors.forename: Jens H
authors.initials: JH
authors.lastname: Henriksen
mesh_terms: D000328:Adult; D000368:Aged; D001692:Biological Transport; D016022:Case-Control Studies; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004912:Erythrocytes / Q000187:drug effects / Q000378:metabolism*; D005260:Female; D005665:Furosemide / Q000494:pharmacology; D006801:Humans; D007700:Kinetics; D008103:Liver Cirrhosis / Q000097:blood* / Q000175:diagnosis; D008297:Male; D008875:Middle Aged; D010042:Ouabain / Q000494:pharmacology; D012964:Sodium / Q000097:blood*; D049994:Sodium Potassium Chloride Symporter Inhibitors / Q000494:pharmacology; D028021:Sodium-Potassium-Chloride Symporters / Q000097:blood / Q000187:drug effects; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors / Q000097:blood
chemical_list: D004791:Enzyme Inhibitors; D049994:Sodium Potassium Chloride Symporter Inhibitors; D028021:Sodium-Potassium-Chloride Symporters; D010042:Ouabain; D005665:Furosemide; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase
keywords: homoeostatic sodium dysregulation; hyponatremia; sodium retention; sodium-potassium ATPase; tracer kinetics