ARGININE DEFICIENCY IN BILE DUCT-LIGATED RATS AFTER SURGERY - THE ROLE OF PLASMA ARGINASE AND GUT ENDOTOXIN RESTRICTION

Citation
Apj. Houdijk et al., ARGININE DEFICIENCY IN BILE DUCT-LIGATED RATS AFTER SURGERY - THE ROLE OF PLASMA ARGINASE AND GUT ENDOTOXIN RESTRICTION, Gastroenterology, 113(4), 1997, pp. 1375-1383
Citations number
36
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
ISSN journal
00165085
Volume
113
Issue
4
Year of publication
1997
Pages
1375 - 1383
Database
ISI
SICI code
0016-5085(1997)113:4<1375:ADIBDR>2.0.ZU;2-M
Abstract
Background & Aims: Arginine deficiency may underlie the cellular immun e depression after surgery in obstructive jaundice, which is associate d with gut-derived endotoxemia. The aim of this study was to study arg inine metabolism in the bile duct-ligated rat (BDL) after laparotomy. Methods: Treatment with cholestyramine, a known endotoxin binder, was used to evaluate the role of gut-derived endotoxemia. Results: In BDL rats arginine levels were lower compared with those in sham-operated c ontrols (P < 0.005), despite a threefold increase in renal arginine re lease (P < 0.01), Liver and gut arginine handling also could not expla in the reduced arginine levels. Higher plasma arginase activity (P < 0 .0001) was measured in BDL rats, explaining both the lower arginine le vels (r = 0.73, P < 0.01) and the increase in arginase product levels: ornithine (P < 0.005 and r = 0.72; P < 0.01) and urea (P < 0.01). Cho lestyramine treatment prevented the decrease in postoperative arginine deficiency by reducing plasma arginase activity by 43% (P < 0.005), I n addition, it significantly lowered plasma levels of the other liver enzymes (aspartate transaminase, alanine transaminase, gamma-glutamyl transpeptidase, and alkaline phosphatase; P < 0.05) in BDL rats. Concl usions: The study concluded that arginine deficiency in BDL rats after surgery is caused by high plasma liver arginase activity, Cholestyram ine prevented the arginine deficiency by reducing plasma arginase acti vity through the inhibition of additional endotoxin-mediated hepatocel lular damage after surgery in BDL rats.