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

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...

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Autores principales: Elman, Robert, McMaster, Philip D.
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 1925
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2130985/
https://www.ncbi.nlm.nih.gov/pubmed/19869039
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author Elman, Robert
McMaster, Philip D.
author_facet Elman, Robert
McMaster, Philip D.
author_sort Elman, Robert
collection PubMed
description 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.
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spelling pubmed-21309852008-04-18 STUDIES ON UROBILIN PHYSIOLOGY AND PATHOLOGY : IV. UROBILIN AND THE DAMAGED LIVER. Elman, Robert McMaster, Philip D. J Exp Med Article 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. The Rockefeller University Press 1925-06-30 /pmc/articles/PMC2130985/ /pubmed/19869039 Text en Copyright © Copyright, 1925, by The Rockefeller Institute for Medical Research New York This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Article
Elman, Robert
McMaster, Philip D.
STUDIES ON UROBILIN PHYSIOLOGY AND PATHOLOGY : IV. UROBILIN AND THE DAMAGED LIVER.
title STUDIES ON UROBILIN PHYSIOLOGY AND PATHOLOGY : IV. UROBILIN AND THE DAMAGED LIVER.
title_full STUDIES ON UROBILIN PHYSIOLOGY AND PATHOLOGY : IV. UROBILIN AND THE DAMAGED LIVER.
title_fullStr STUDIES ON UROBILIN PHYSIOLOGY AND PATHOLOGY : IV. UROBILIN AND THE DAMAGED LIVER.
title_full_unstemmed STUDIES ON UROBILIN PHYSIOLOGY AND PATHOLOGY : IV. UROBILIN AND THE DAMAGED LIVER.
title_short STUDIES ON UROBILIN PHYSIOLOGY AND PATHOLOGY : IV. UROBILIN AND THE DAMAGED LIVER.
title_sort studies on urobilin physiology and pathology : iv. urobilin and the damaged liver.
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2130985/
https://www.ncbi.nlm.nih.gov/pubmed/19869039
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