A study in vitro of the sodium pump in fulminant hepatic failure.
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.
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
D000255:Adenosine Triphosphate; D012964:Sodium; D000252:Calcium-Transporting ATPases; D000254:Sodium-Potassium-Exchanging ATPase