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To identify factors affecting bilirubin excretion, the effects of bile flow and bile salt excretion on bilirubin output into bile have been examined in normobilirubinemic, cholecystectomized patients with balloon-occludable, reinfusion T-tubes, 8 patients with cholesterol (CS) and 2 with pigment (PS) gallstones. Another patient with pigment gallstones, sickle cell disease (SS), and stable jaundice was studied to examine the mechanism by which an increased bilirubin load was excreted. Total bilirubin was almost entirely conjugated and excretion was related linearly to bile salt excretion in PS and CS subjects; one-third of bilirubin excretion was bile salt independent and two-thirds was bile salt associated. In the SS patient 90% of the bilirubin excretion was independent of bile salt output. In PS and CS patients, bilirubin output was linearly related to bile flow, but the SS patient showed significant bilirubin excretion at low flow rates. CS and PS patients had similar patterns of bilirubin excretion, but the increased bilirubin load in the SS patient was excreted entirely independently of bile salts. In the SS patient, unconjugated bilirubin output was hyperbolically related to bile salt output and represented a maximum of 3% of the total bilirubin output. The bile salt-independent excretion of conjugated bilirubin suggests that micelles were not required for transport into bile; whereas the hyperbolic relationship for unconjugated bilirubin and bile salt output, similar to that of the micellar lipids, cholesterol, and phospholipids, suggests interaction with micelles.

Studies utilizing balloon-occludable T or duodenal tubes in subjects with and without gallbladders were undertaken to identify the contribution of the gallbladder, the sphincter of Oddi, and bile salts to the delivery of bile to the duodenum. Patients with and without a functional sphincter of Oddi and with and without a gallbladder were compared. The presence of a functional sphincter of Oddi in duodenal tube patients reduced bile salt output by more than 67% from that observed in T-tube patients. When cholecystectomized and normal patients were compared using the duodenal tube, peak bile salt output was significantly increased in normal subjects, reflecting gallbladder contraction, but total bile salt output was not significantly increased suggesting that the gallbladder has a minor role in bile delivery. Exogenous infusion of cholecystokinin produced much more stable bile secretion than did endogenous release of cholecystokinin by intraduodenal infusion of essential amino acids. This rhythmic release of bile after endogenous cholecystokinin release was related to the concentration of bile salts in the intestinal lumen. Thus, delivery of bile to the duodenum is wave-like and is predominantly controlled by the sphincter of Oddi.