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A B S T R A C T Hydrocortisone sodium succinate (SoluCortef; Upjohn Co., Kalamazoo, Mich.) has been found to induce choleresis in unanesthetized fasting dogs fitted with Thomas duodenal cannulae for direct quantitative collection of bile. In all experiments, bile flow increased (average, 68%) 15-20 min after beginning hydrocortisone by infusion in association with an equivalent increment in the output of sodium, potassium, chloride, and bicarbonate. In five animals, the choleretic response occurred independently of, and apparently additive to, the effect of simultaneously administered sodium taurocholate. The fluid added to the bile resembled an ultrafiltrate of plasma. Erythritol clearance increased in proportion to flow, suggesting an effect at the hepatocellular rather than ductal level and probably independent, therefore, of endogenous secretin release. Hydrocortisone and its metabolites were excreted in amounts too small to induce choleresis osmotically. Simultaneous administration of sulfobromophthalein sodium blocked the choleretic response without preventing hydrocortisone excretion. The data suggest that a previously ill-defined mechanism of canalicular bile formation, not mediated by bile salt excretion, may be operative in choleretic response to a variety of agents.

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