The 6th meeting was held in London on 2, 3, and 4 September under the presidency of B. H. Billing (United Kingdom). The following are the abstracts of the first 36 papers. Altogether 157 abstracts were submitted but only those which were read at the meeting are reprinted in Gut. The remainder can be found in the booklet of abstracts which each member received at the meeting. The conference of the EASL was preceded by a meeting of the Liver Club. Recent experimental reports support the

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... that a large fraction of hepatocytic bile is not dependent on bile salt excretion. However, the mechanism of elaboration of this fraction is not established. Suppression of this bile salt-independent flow in the rabbit by inhibitors of sodium transport suggests that it may be the result of active sodium transport by the hepatocytes. These studies were undertaken to examine the influence on bile formation in the dog of theophylline, an agent known to stimulate sodium transport. In ten anaesthetized dogs, the bile duct was cannulated, a bile salt infusion (6 gmoles/min) was given to obtain a stable bile flow. (1) Theophylline (280 j,umoles followed by a constant infusion of 20 ,moles/min) produced a significant increase in bile flow, from an average control value of 0.165 ± (1 SD) 0.070 ml/min to 0.294 ± 0.073 ml/min (p < 0-005). (2) Bile salt concentration in bile decreased significantly from 55.9 ± 22.9 mmoles/l to 30.4 ± 14.7 mmoles/l (p < 0005). (3) Bile salt excretion rate was not significantly modified. (4) 14C-erythritol clearance increased in proportion to bile flow, indicating that choleresis was of hepatocellular rather than ductular origin. (5) 3H-labelled theophylline, given intravenously, was excreted in bile and allowed quantitative estimation of the amount of theophylline recovered in bile: in two dogs, during the 80 minutes following an injection of 560 ,moles of theophylline, the mean biliary excretion of the drug was 0.09 and 0.12 ,umoles/min, an amount too small to produce an osmotic choleresis. (6) Sodium excretion in bile increased and a linear relationship was obtained between sodium excretion and bile flow. These studies support the postulate that, in the dog, the bile salt independent fraction of bile could be the result of active sodium transport by the hepatocytes. 2