THE HUMAN GALLBLADDER INCREASES CHOLESTEROL SOLUBILITY IN BILE BY DIFFERENTIAL LIPID ABSORPTION - A STUDY USING A NEW IN-VITRO MODEL OF ISOLATED INTRAARTERIALLY PERFUSED GALLBLADDER

In this study, we first developed and validated a new in vitro isolate d, intra-arterially perfused, gallbladder model and then applied the m ethod to investigate the absorption of biliary lipids by the gallbladd er wall and the effect of this process on the composition of human bil e. Oxygenated and glucose-added buffer was perfused through the cystic artery to maintain organ viability. A standard pooled natural bile, r adiolabeled with H-3-cholesterol and C-14-palmitoyl-linoleoyl-phosphat idylcholine, was instilled in the lumen via a cystic duct catheter. Ch anges in bile volume and lipid concentrations were monitored at time i ntervals to evaluate the disappearance of lipids from bile caused by g allbladder absorptive function. Organ viability was demonstrated by st able lactate dehydrogenase (LDH) organ release and oxygen consumption throughout the experiments. In the pig, disappearance rates of lipids from bile were similar in vitro and in vivo, demonstrating the validit y of the isolated in vitro model for functional studies. By applying o ur in vitro isolated preparation to the human gallbladder, we found th at 23% of cholesterol and 32% of phosphatidylcholine, but only 9% of b ile salts, disappeared from bile in 5 hours. As a consequence, at the end of the experiments, cholesterol (P < .05) and phospholipid (P < .0 5) molar percentages were significantly reduced, while the bile salt ( P < .05) molar percentage was significantly increased with respect tc, values at the beginning of the studies. Our findings are of pathophys iological relevance and support the concept that the human gallbladder modifies the relative composition of biliary lipids in such a way as to increase cholesterol solubility in bile.