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Summary: An experimental model, originally designed to study the effects of controlled interruption of the enterohepatic circulation (EHC), has been extensively modified and adapted to study the applied physiology of an “intact” EHC of bile in Rhesus monkeys. Basically, the model consists of a surgically exteriorised extrahepatic biliary circuit in which an electronic stream splitter is interposed. This diverts every twentieth drop of bile which provides a representative sample for analysis while returning the remaining 95% of bile to the upper intestine. During these studies, the monkeys were comfortably restrained in specially designed chairs whose construction is described in detail. Animal maintenance and the design of the electronic stream splitter are also described. Analysis of the glycine: taurine and the dihydroxy: trihydroxy bile salt ratios both in gallbladder bile and in bile obtained with an “intact” EHC (by using the stream splitter), showed that the Rhesus monkey secretes a bile similar in composition to that of man. The bile salt: cholesterol: phospholipid ratios in monkey gallbladder bile (81:6:13) were also similar to those found in human bile, indicating that this animal is suitable for studies of cholesterol solubility in bile – a factor of major importance in gallstone pathogenesis. The model has been used to measure bile volume, bile salt secretion, pool size and the frequency of circulation of the bile salt pool. The diurnal variation in these variables has also been studied.

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The reactions which result in the conversion of pregnenolone to progesterone and of progesterone to deoxycorticosterone in undisrupted microsomal preparations from rat adrenal glands were stimulated by homologous serum. The active materials were shown to be firmly associated with serum proteins. The dialysable fraction of serum was either without effect on these transformations or was inhibitory. The enzyme systems involved were partially solubilized by exposure of the microsomal preparation to prolonged sonic treatment or to 1% Triton N-101. After either treatment, 35-40% of the original specific activity of the steroid 21-hydroxylase system responsible for the conversion of progesterone to deoxycorticosterone was found in the supernatant fraction after high-speed centrifuga-J Reprint requests to S. R. hydroxysteroid dehydrogenase activity, but did not activate 5-ene-3oxosteroid isomerase in the microsomal fraction. This finding suggested that activation of 5-ene-3/?-hydroxysteroid dehydrogenase was responsible for stimulation of progesterone synthesis from pregnenolone. The results indicate that the protein-bound factor in rat serum which was capable of stimulating the conversion of progesterone to deoxycorticosterone in microsomal preparations from rat adrenal glands was different from that which activates the conversion of pregnenolone to progesterone. Moreover, these diverse factors appeared to act by different mechanisms.-60°C. The frozen

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