Linked Life Data

6724187

Source:http://linkedlifedata.com/resource/pubmed/id/6724187

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2 Pt 1
pubmed:dateCreated
1984-7-2
pubmed:abstractText
Since alcoholism is a major health problem, mechanisms responsible for various forms of alcoholic liver disease (e.g., fatty liver, alcoholic hepatitis, and cirrhosis) require elucidation. Knowledge of these mechanisms is needed to provide a sound framework to treat alcoholic liver disease, to prevent its occurrence and to identify those most susceptible to it. Israel and co-workers proposed that ethanol-induced necrosis results from hypoxia to centrilobular hepatocytes as a consequence of an alcohol-induced increase in hepatic oxygen utilization (Y. Israel, H. Kalant , H. Orrego , J. M. Khanna , L. Videla , and J. M. Phillips, 1975, Proc. Natl. Acad. Sci. USA, 72(3), 1137-1141). We have employed several new techniques to evaluate this hypothesis. Procedures have been developed to make measurements of hepatic metabolism within the hepatic lobule in the isolated, perfused liver using miniature light guides and oxygen electrodes. By comparing these lobular measurements to global metabolism and to hepatic morphology determined by light and electron microscopy, a coherent, quantitative description of lobular oxygen metabolism is emerging. With these techniques, the lobular oxygen gradient was measured directly in isolated, perfused rat livers. This gradient was elevated in livers from ethanol-treated rats, an effect which was blocked by the antithyroid drug, propylthiouracil. Restriction of oxygen delivery to the isolated liver produced stable, circumscribed zones of virtual anoxia localized around the central vein. Anoxic stress led within minutes to centrilobular injury with complete sparing of periportal areas. Cellular injury was characterized by the formation of membranous blebs on the surface of centrilobular hepatocytes. When hypoxic tissue was reoxygenated , blebs were released into the circulation.(ABSTRACT TRUNCATED AT 250 WORDS)
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0272-0590
pubmed:author
pubmed:issnType
Print
pubmed:volume
4
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
125-33
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1984
pubmed:articleTitle
Is hypoxia involved in the mechanism of alcohol-induced liver injury?
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't