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THE RELATIONSHIP BETWEEN THE VASCULAR MANIFESTATIONS OF SHOCK PRODUCED BY ENDOTOXIN, TRAUMA, AND HEMORRHAGE : II. THE POSSIBLE ROLE OF THE RETICULO-ENDOTHELIAL SYSTEM IN RESISTANCE TO EACH TYPE OF SHOCK
In studies designed to establish the interrelationship between bacterial endotoxins and the vascular sequelae of hemorrhagic and traumatic shock, the effect of factors known to influence the phagocytic behavior of the reticulo-endothelial system (RES) were investigated. Measures which induced a so c...
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Formato: | Texto |
Lenguaje: | English |
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The Rockefeller University Press
1957
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2136771/ https://www.ncbi.nlm.nih.gov/pubmed/13463250 |
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author | Zweifach, Benjamin W. Benacerraf, Baruj Thomas, Lewis |
author_facet | Zweifach, Benjamin W. Benacerraf, Baruj Thomas, Lewis |
author_sort | Zweifach, Benjamin W. |
collection | PubMed |
description | In studies designed to establish the interrelationship between bacterial endotoxins and the vascular sequelae of hemorrhagic and traumatic shock, the effect of factors known to influence the phagocytic behavior of the reticulo-endothelial system (RES) were investigated. Measures which induced a so called "blockade" of the RES were uniformly associated with an exacerbation of the vascular effects of the endotoxin of E. coli. Such pretreatment also counteracted the cross-tolerance induced by endotoxins against the lethal effects of hemorrhage or drum trauma. The vascular reactions characteristic of irreversible hemorrhagic shock could be simulated by a combination of pretreatment with carbon or proferrin and the infusion of small doses of E. coli endotoxin. An increase in the phagocytic activity of the RES, induced by repeated injections of certain colloids, was associated with an enhanced tolerance of shock. Measurement of carbon clearance values indicated that although an augmented phagocytic capacity was present in rats with induced tolerance to bacterial endotoxins, the development of resistance to trauma was not associated with a comparable change in the phagocytic function of the RES. |
format | Text |
id | pubmed-2136771 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1957 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21367712008-04-17 THE RELATIONSHIP BETWEEN THE VASCULAR MANIFESTATIONS OF SHOCK PRODUCED BY ENDOTOXIN, TRAUMA, AND HEMORRHAGE : II. THE POSSIBLE ROLE OF THE RETICULO-ENDOTHELIAL SYSTEM IN RESISTANCE TO EACH TYPE OF SHOCK Zweifach, Benjamin W. Benacerraf, Baruj Thomas, Lewis J Exp Med Article In studies designed to establish the interrelationship between bacterial endotoxins and the vascular sequelae of hemorrhagic and traumatic shock, the effect of factors known to influence the phagocytic behavior of the reticulo-endothelial system (RES) were investigated. Measures which induced a so called "blockade" of the RES were uniformly associated with an exacerbation of the vascular effects of the endotoxin of E. coli. Such pretreatment also counteracted the cross-tolerance induced by endotoxins against the lethal effects of hemorrhage or drum trauma. The vascular reactions characteristic of irreversible hemorrhagic shock could be simulated by a combination of pretreatment with carbon or proferrin and the infusion of small doses of E. coli endotoxin. An increase in the phagocytic activity of the RES, induced by repeated injections of certain colloids, was associated with an enhanced tolerance of shock. Measurement of carbon clearance values indicated that although an augmented phagocytic capacity was present in rats with induced tolerance to bacterial endotoxins, the development of resistance to trauma was not associated with a comparable change in the phagocytic function of the RES. The Rockefeller University Press 1957-09-01 /pmc/articles/PMC2136771/ /pubmed/13463250 Text en Copyright © Copyright, 1957, 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 Zweifach, Benjamin W. Benacerraf, Baruj Thomas, Lewis THE RELATIONSHIP BETWEEN THE VASCULAR MANIFESTATIONS OF SHOCK PRODUCED BY ENDOTOXIN, TRAUMA, AND HEMORRHAGE : II. THE POSSIBLE ROLE OF THE RETICULO-ENDOTHELIAL SYSTEM IN RESISTANCE TO EACH TYPE OF SHOCK |
title | THE RELATIONSHIP BETWEEN THE VASCULAR MANIFESTATIONS OF SHOCK PRODUCED BY ENDOTOXIN, TRAUMA, AND HEMORRHAGE : II. THE POSSIBLE ROLE OF THE RETICULO-ENDOTHELIAL SYSTEM IN RESISTANCE TO EACH TYPE OF SHOCK |
title_full | THE RELATIONSHIP BETWEEN THE VASCULAR MANIFESTATIONS OF SHOCK PRODUCED BY ENDOTOXIN, TRAUMA, AND HEMORRHAGE : II. THE POSSIBLE ROLE OF THE RETICULO-ENDOTHELIAL SYSTEM IN RESISTANCE TO EACH TYPE OF SHOCK |
title_fullStr | THE RELATIONSHIP BETWEEN THE VASCULAR MANIFESTATIONS OF SHOCK PRODUCED BY ENDOTOXIN, TRAUMA, AND HEMORRHAGE : II. THE POSSIBLE ROLE OF THE RETICULO-ENDOTHELIAL SYSTEM IN RESISTANCE TO EACH TYPE OF SHOCK |
title_full_unstemmed | THE RELATIONSHIP BETWEEN THE VASCULAR MANIFESTATIONS OF SHOCK PRODUCED BY ENDOTOXIN, TRAUMA, AND HEMORRHAGE : II. THE POSSIBLE ROLE OF THE RETICULO-ENDOTHELIAL SYSTEM IN RESISTANCE TO EACH TYPE OF SHOCK |
title_short | THE RELATIONSHIP BETWEEN THE VASCULAR MANIFESTATIONS OF SHOCK PRODUCED BY ENDOTOXIN, TRAUMA, AND HEMORRHAGE : II. THE POSSIBLE ROLE OF THE RETICULO-ENDOTHELIAL SYSTEM IN RESISTANCE TO EACH TYPE OF SHOCK |
title_sort | relationship between the vascular manifestations of shock produced by endotoxin, trauma, and hemorrhage : ii. the possible role of the reticulo-endothelial system in resistance to each type of shock |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2136771/ https://www.ncbi.nlm.nih.gov/pubmed/13463250 |
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