Sodium transport in the diseased human gallbladder and the effects of indomethacin.
1. Sodium ion (Na+) transport, a principal function of the gallbladder epithelium, was studied by measuring the flux of 22Na across isolated, inflamed human gallbladder mucosa maintained in a modified 'Ussing' flux chamber. Tissue was obtained from cholecystectomy specimens in symptomatic patients with cholelithiasis. 2. In 30 gallbladders studied, 57% had a net Na+ flux from mucosa to serosa (Na+ absorption), while 23% had a net Na+ flux from serosa to mucosa (Na+ secretion). The remaining 20% showed no overall net Na+ flux. 3. Indomethacin added to the serosal fluid reversed the direction of net Na+ flux in secreting gallbladders and caused an absorption of Na+. In Na+-absorbing gallbladders, indomethacin caused a slight reduction in Na+ absorption. No change in Na+ flux was induced in gallbladders with no initial net Na+ flux. 4. These results demonstrate that instead of absorbing Na+, some inflamed human gallbladders may secrete Na+. As this secretion can be reversed to the more usual absorption by indomethacin, it is likely that this secretion is mediated by prostaglandins.
Jacyna
M R
MR
Department of Medicine, Ninewells Hospital and Medical School, Dundee, Scotland, U.K.
Ross
P E
PE
Hopwood
D
D
Bouchier
I A
IA
D001693:Biological Transport, Active; D002769:Cholelithiasis / Q000378:metabolism*; D005704:Gallbladder / Q000187:drug effects*; D006801:Humans; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology*; D012964:Sodium / Q000378:metabolism*
D012964:Sodium; D007213:Indomethacin