• Login
    View Item 
    •   Home
    • UA Graduate and Undergraduate Research
    • UA Theses and Dissertations
    • Dissertations
    • View Item
    •   Home
    • UA Graduate and Undergraduate Research
    • UA Theses and Dissertations
    • Dissertations
    • View Item
    JavaScript is disabled for your browser. Some features of this site may not work without it.

    Browse

    All of UA Campus RepositoryCommunitiesTitleAuthorsIssue DateSubmit DateSubjectsPublisherJournalThis CollectionTitleAuthorsIssue DateSubmit DateSubjectsPublisherJournal

    My Account

    LoginRegister

    About

    AboutUA Faculty PublicationsUA DissertationsUA Master's ThesesUA Honors ThesesUA PressUA YearbooksUA CatalogsUA Libraries

    Statistics

    Most Popular ItemsStatistics by CountryMost Popular Authors

    Oxygen radicals and liver injury in hemorrhagic shock and resuscitation

    • CSV
    • RefMan
    • EndNote
    • BibTex
    • RefWorks
    Thumbnail
    Name:
    azu_td_9123472_sip1_m.pdf
    Size:
    3.473Mb
    Format:
    PDF
    Description:
    azu_td_9123472_sip1_m.pdf
    Download
    Author
    Dart, Richard Charles
    Issue Date
    1991
    Keywords
    Dissertations, Academic
    Hemorrhagic shock
    Molecular biology -- Research
    Advisor
    Liebler, Daniel
    
    Metadata
    Show full item record
    Publisher
    The University of Arizona.
    Rights
    Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
    Abstract
    Hemorrhagic shock is a clinical syndrome involving widespread cellular dysfunction and resulting in injury to many organs. Resuscitation from hemorrhagic shock is similar to reperfusion after ischemia, but differs in that some blood flow persists during shock. Ischemia-reperfusion produces oxygen radicals in many organs, including the liver of the rat and the human. The hypothesis of this project was that oxygen radicals are produced and cause hepatic injury during resuscitation from hemorrhagic shock. The production of oxygen radicals within the liver should cause lipid peroxidation and tissue injury. Manipulation of defenses against oxygen radicals should decrease the hepatic injury caused by hemorrhagic shock and resuscitation. The blood pressure of Sprague-Dawley rats was reduced to 35-40 mm Hg by blood withdrawal for two hours, followed by reinfusion of withdrawn blood. Plasma alanine aminotransferase (ALT) levels rose and injury to hepatocytes and non-parenchymal cells was found on transmission electron microscopy. The presence of lipid peroxidation was determined by quantitation of ethane exhalation and hepatic content of thiobarbituric acid reactive substances (TBARS). Ethane exhalation was elevated during the hypotensive phase and after resuscitation. Hepatic TBARS levels were elevated after resuscitation only. The same hemorrhagic shock protocol was used to determine the effect of antioxidant manipulation on hepatic injury. The antioxidants superoxide dismutase, catalase, or deferoxamine produced no reduction in hepatic injury. The administration of phorone reduced hepatic non-protein sulfhydryl content and increased plasma ALT levels nine fold at 24 hours after resuscitation. The development of lipid peroxidation and the exacerbation of liver injury by the administration of phorone suggest that oxygen radicals are produced in the liver during hemorrhagic shock and resuscitation. However, the administration of antioxidants provided no protection. Therefore, it seems unlikely the oxygen radicals are involved in the pathogenesis of liver injury in this model. It is possible that the lipid peroxidation occurs after the cell is irreversible injured.
    Type
    text
    Dissertation-Reproduction (electronic)
    Degree Name
    Ph.D.
    Degree Level
    doctoral
    Degree Program
    Pharmacology & Toxicology
    Graduate College
    Degree Grantor
    University of Arizona
    Collections
    Dissertations

    entitlement

     
    The University of Arizona Libraries | 1510 E. University Blvd. | Tucson, AZ 85721-0055
    Tel 520-621-6442 | repository@u.library.arizona.edu
    DSpace software copyright © 2002-2017  DuraSpace
    Quick Guide | Contact Us | Send Feedback
    Open Repository is a service operated by 
    Atmire NV
     

    Export search results

    The export option will allow you to export the current search results of the entered query to a file. Different formats are available for download. To export the items, click on the button corresponding with the preferred download format.

    By default, clicking on the export buttons will result in a download of the allowed maximum amount of items.

    To select a subset of the search results, click "Selective Export" button and make a selection of the items you want to export. The amount of items that can be exported at once is similarly restricted as the full export.

    After making a selection, click one of the export format buttons. The amount of items that will be exported is indicated in the bubble next to export format.