BILIARY DECOMPRESSION PROMOTES KUPFFER CELL RECOVERY IN OBSTRUCTIVE-JAUNDICE

Background-Jaundiced patients undergoing surgical procedures have an i ncreased risk of Gram negative sepsis with potential morbidity and mor tality. Depressed Kupffer cell clearance capacity (KCCC) predisposes j aundiced patients to endotoxaemia and its sequelae. Biliary decompress ion remains the main therapeutic strategy in obstructive jaundice. Aim s-This study investigates the efficacy of internal (ID) and external b iliary drainage (ED) on KCCC in an experimental model of extrahepatic biliary obstruction. Methods-Adult male Wistar rats (250-300 g) were a ssigned to one of six groups: sham operated, where the bile duct was m obilised but not divided; bile duct ligation (BDL) for three weeks, an d sham operated or BDL for three weeks followed by a second laparotomy and further 21 days of ID or ED, by way of choledochoduodenostomy or choledochovesical fistula respectively. KCCC was measured using an iso lated hepatic perfusion technique with FITC labelled latex particles ( 0.75 mu) as the test probe. Plasma was assayed for bilirubin, endotoxi n, and anticore glycolipid antibody (ACGA) concentrations. Results-Jau ndiced rats had reduced KCCC (p<0.001), increased concentrations of AC GA (p<0.001), and endotoxin (p<0.001) compared with controls. Biliary drainage for three weeks produced a recovery in KCCC and normalisation of endotoxin and ACGA concentrations, however, external drainage was less effective than ID (p<0.01). Conclusions-These data support the hy pothesis that endotoxaemia and its mediated effects are integral in th e pathophysiology of jaundice. Furthermore, a short period of internal biliary drainage is a useful therapeutic strategy in restoring Kupffe r cell function and negating systemic endotoxaemia and consequent comp lications in biliary obstruction.