Jesse L. Bollman

Identification of extrahepatic bilirubin monoglucuronide and its conversion to pigment 2 by isolated liver.

Summary and Conclusions The pigment obtained by reversed-phase partition chromatography from the plasma of the hepatectomized dog has been shown to be bilirubin monoglucuronide (pigment 1). In the experiments performed, pigment 1 was of extrahepatic origin. The isolated perfused rat liver converts bilirubin monoglucuronide to bilirubin diglucuronide and excretes the diconjugate in the bile.

Metabolic pathways of tetraiodothyroacetic acid, triiodothyroacetic acid, tetraiodothyropropionic acid and triiodothyropropionic acid☆☆☆

Abstract Major metabolic pathways for l -thyroxine and l -3,5,3-triiodothyronine involve removal of an iodine atom from the benzene ring with the side chain and thus inactivation of these hormones. Conjugates of the products 3,3,5-triiodothyronine and 3,3-diiodothyronine are excreted in the bile of dogs with livers but accumulate in the blood and urine of dogs without livers. Analogs of the thyroid hormones labeled with 131 I in the 3 or 5 position were studied in dogs with biliary fistulas and in hepatectomized dogs. In dogs with biliary fistulas tetraiodothyroacetic acid was metabolized much more slowly than was thyroxine ; much less 131 I was excreted in bile or urine. Large amounts of unchanged tetraiodothyroacetic acid with smaller amounts of 3,3,5-triiodothyroacetic acid were found in the blood. Tetraiodothyropropionic acid was partially deiodinated to 3,3,5-triiodothyropropionic acid which accumulated in the blood as the amount of unchanged tetraiodothyropropionic acid decreased. Both of these compounds of propionic acid were excreted in bile as glucosiduronides. 3,5,3-Triiodothyroacetic acid and 3,5,3-triiodothyropropionic acid were rapidly cleared from the blood and excreted in the bile chiefly as glucosiduronides, with small amounts of the ethereal sulfate conjugates of 3,3-diiodothyroacetic acid and 3,3-diiodothyropropionic acid. In dogs without livers, the sulfates of these 3,3-diiodo-compounds were found in larger amounts in both blood and urine, but the major metabolites appeared to be sulfoconjugates of 3-monoiodo-derivatives.

Further studies on the nature and source of the conjugated bile pigments.

Summary and conclusions Rat-fistula bile, isolated rat liver, liver slices incubated with bilirubin, and the hepatectomized dog were utilized to study the nature and sources of conjugated bile pigment. The technics of reverse-phase column chromatography, chemical-partition chromatography, and paper chromatography were employed and molar ratios were calculated. Probably pigment 1 is formed solely in extrahepatic sites. The evidence favors a bilirubin monoglucuronide structure for pigment 1 rather than a complex of bilirubin and pigment 2. In the dog, pigment 2 probably is formed only within the liver. It is suggested that bilirubin diglucuronide may be formed intrahepatically from bilirubin directly, as well as from part of the extrahepatic pigment 1.

Pressures in the common hepatic duct of the rat.

Summary 1) A method for recording pressure within the common hepatic duct of the rat with a strain-gauge manometer is described. Measurements of pressure in the common hepatic duct were made on a series of fasting rats with normal livers, cirrhosis or passive venous congestion of the liver, and these were analyzed statistically. The higher mean secretory pressure in the rat with cirrhosis over that in the rat with normal liver and with passive venous congestion is statistically significant. 2) Secretory pressure in rats after inhalation of carbon tetrachloride vapor fell slightly but significantly. 3) The duodenal-end pressure in the common hepatic duct was related to findings on simultaneous recordings of biliary pressure and gastric and duodenal motility. This pressure was significantly higher in rats with chronic venous congestion of the liver than in normal or cirrhotic animals. The lower end of the common hepatic duct probably has some sphincteric action in the rat. 4) Intravenous injection of chlorpromazine hydrochloride (thorazine) produced no effects on pressure in the common hepatic duct in normal rats.

The diarrhea of the pancreatic insufficiency

to the patient those foods which he should eat rather than to place emphasis, as has been done for generations, on those foods which he should not eat. Dr. Jones raised the question of disturbance of the colon in relation to deficiency states. In two of our cases we found evidence of chronic ulcerative colitis. What the relationship may be between disease of the colon and deficiency states, in other words, which is primary and which is secondary, is impossible to state in many instances.

Turnover Rate of Phospholipid Phosphorus in the Liver of the White Rat

Conclusions The proportional turnover rate R for hepatic phospholipid P in the white rat is on the average close to 5% per hour, and since the mean concentration of hepatic phospholipid P for both experiments together was 132 mg per 100 g of liver, that r, the mass turnover rate, is about 6 mg P per hour per 100 g of liver, which is 0.2 mg P per 100 g body weight.