Literature DB >> 19869039

STUDIES ON UROBILIN PHYSIOLOGY AND PATHOLOGY : IV. UROBILIN AND THE DAMAGED LIVER.

R Elman1, P D McMaster.   

Abstract

A variety of evidence is presented, all of which supports the view that in the uninfected animal the intestinal tract is the only place of origin of urobilin, not merely under normal circumstances, but when there is biliary obstruction. Animals rendered urobilin-free by collection of all of the bile from the intubated common duct remain urobilin-free even after severe hepatic injury. In our experiments urobilinuria was never found after liver damage except when bile pigment was present in the intestine. Thus, for example, it appeared during the first days after Ugation of the common duct, but disappeared as the stools became acholic. When this had happened a small amount of urobilin-free bile, given by mouth, precipitated a prompt urobilinuria. After obstruction of the duct from one-third of the liver, mild urobilinuria was found, but no bilirubinuria. In animals intubated for the collection of a part of the bile only, while the rest flowed to the duodenum through the ordinary channels, liver injury caused urobilinuria, unless indeed it was so severe as to lead to bile suppression, when almost at once the urobilinuria ceased, though the organism became jaundiced. The evidence here presented, when taken with that of our previous papers, clearly proves that urobilinuria is an expression of the inability of the liver cells to remove from circulation the urobilin brought by the portal stream, with result that the pigment passes on to kidney and urine. Urobilinuria occurs with a far less degree of liver injury than does bilirubinuria. Our work has, for the most part, been carried out with animals having uninfected livers and bile passages. But the influence of cholangitis with infection has been briefly discussed in the light of some preliminary observations. The influence of infection on the place of formation of urobilin and on the occurrence of urobilinuria will form the subject of another communication.

Entities:  

Year:  1925        PMID: 19869039      PMCID: PMC2130985          DOI: 10.1084/jem.42.1.99

Source DB:  PubMed          Journal:  J Exp Med        ISSN: 0022-1007            Impact factor:   14.307


  8 in total

1.  STUDIES ON THE TOTAL BILE : III. ON THE BILE CHANGES CAUSED BY A PRESSURE OBSTACLE TO SECRETION; AND ON HYDROHEPATOSIS.

Authors:  P D McMaster; G O Broun; P Rous
Journal:  J Exp Med       Date:  1923-04-30       Impact factor: 14.307

2.  AN EXPERIMENTAL STUDY OF THE METABOLISM AND PATHOLOGY OF DELAYED CHLOROFORM POISONING.

Authors:  J Howland; A N Richards
Journal:  J Exp Med       Date:  1909-03-01       Impact factor: 14.307

3.  THE RELATION BETWEEN BLOOD DESTRUCTION AND THE OUTPUT OF BILE PIGMENT.

Authors:  G O Broun; P D McMaster; P Rous
Journal:  J Exp Med       Date:  1923-05-31       Impact factor: 14.307

4.  SUPPRESSION OF BILE AS A RESULT OF IMPAIRMENT OF LIVER FUNCTION.

Authors:  D R Drury; P Rous
Journal:  J Exp Med       Date:  1925-04-30       Impact factor: 14.307

5.  STUDIES ON UROBILIN PHYSIOLOGY AND PATHOLOGY : III. ABSORPTION OF PIGMENTS OF BILIARY DERIVATION FROM THE INTESTINE.

Authors:  P D McMaster; R Elman
Journal:  J Exp Med       Date:  1925-05-31       Impact factor: 14.307

6.  RELATION OF THE PORTAL BLOOD TO LIVER MAINTENANCE : A DEMONSTRATION OF LIVER ATROPHY CONDITIONAL ON COMPENSATION.

Authors:  P Rous; L D Larimore
Journal:  J Exp Med       Date:  1920-04-30       Impact factor: 14.307

7.  STUDIES ON UROBILIN PHYSIOLOGY AND PATHOLOGY : I. THE QUANTITATIVE DETERMINATION OF UROBILIN.

Authors:  R Elman; P D McMaster
Journal:  J Exp Med       Date:  1925-03-31       Impact factor: 14.307

8.  THE BILIARY OBSTRUCTION REQUIRED TO PRODUCE JAUNDICE.

Authors:  P D McMaster; P Rous
Journal:  J Exp Med       Date:  1921-05-31       Impact factor: 14.307

  8 in total

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