title: A study in vitro of the sodium pump in fulminant hepatic failure.
abstract: 1. The mechanism underlying the raised leucocyte sodium content in fulminant hepatic failure was studied by measurement of sodium fluxes, (Na+ + K+)-dependent adenosine triphosphatase activity, and leucocyte ATP content. 2. The rate constant for sodium efflux in the leucocytes was significantly reduced, and attributable to reduced activity of the enzyme (Na+ + K+)-ATPase. Leucocyte ATP content was not significantly different from that of control cells. 3. Incubation of cells from patients in the sera of normal subjects resulted in a reversal of these changes. Inhibition of the leucocyte sodium efflux rate constants and (Na+ +K+)-ATPase of normal cells was achieved by incubation in sera from patients. 4. We suggest that the raised sodium content of leucocytes in fulminant hepatic failure is attributable to a defective sodium pumping mechanism, possibly due to a circulating toxin.
mesh_terms: D000255:Adenosine Triphosphate / Q000097:blood; D000293:Adolescent; D000328:Adult; D001693:Biological Transport, Active; D000252:Calcium-Transporting ATPases / Q000097:blood; D005260:Female; D006801:Humans; D007962:Leukocytes / Q000378:metabolism; D008107:Liver Diseases / Q000097:blood*; D008297:Male; D008875:Middle Aged; D011247:Pregnancy; D012964:Sodium / Q000097:blood*; D000254:Sodium-Potassium-Exchanging ATPase / Q000097:blood
chemical_list: D000255:Adenosine Triphosphate; D012964:Sodium; D000252:Calcium-Transporting ATPases; D000254:Sodium-Potassium-Exchanging ATPase