Document Detail


Activated neutrophils injure the isolated, perfused rat liver by an oxygen radical-dependent mechanism.
MedLine Citation:
PMID:  1951624     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Under certain circumstances, segmented neutrophils (PMNs) injure extrahepatic tissue by releasing toxic oxygen species and degradative enzymes. The authors used an isolated, perfused rat liver preparation to determine whether PMNs might injure the liver. Livers from fasted rats were perfused with Krebs-Ringer bicarbonate buffer (pH 7.4) containing 3% bovine serum albumin (BSA) in a recirculating system. Rat peritoneal PMNs (4 x 10(8] or vehicle (Hank's balanced salt solution [HBSS], pH 7.35) were added, and liver injury was assessed 90 minutes later by release of alanine aminotransferase (ALT) into the perfusion medium and histopathologic analysis of liver sections. Perfusion of livers receiving only HBSS for 90 minutes resulted in a small increase in ALT activity in the perfusion medium but did not significantly alter histologic features of liver sections. Addition of unstimulated PMNs did not increase further the ALT activity and, with the exception of vascular neutrophilia, did not significantly change the histomorphology compared with controls. When PMNs activated with a combination of phorbol myristate acetate (PMA, 31 ng/ml) and lithocholate (100 mumol/l [micromolar]) were added to the perfusion system, however, livers released greater amounts of ALT than those perfused with PMA, lithocholate, and HBSS. Activated PMNs caused a transient reduction in flow of perfusion medium that lasted approximately 5 to 15 minutes. Liver sections had multifocal to coalescing foci of moderate to severe, acute hepatocellular necrosis associated with the areas of intense sinusoidal neutrophilia. In addition a second type of lesion was observed and was characterized by triangular foci of necrosis located adjacent to periportal regions of sinusoids or portal veins containing neutrophilic thrombi. These lesions were void of PMNs and were consistent with infarcts. A combination of superoxide dismutase and catalase added to the perfusion medium (500 U/ml each) prevented the elevation in ALT activity but not the transient reduction in flow. These results indicate that activated PMNs may cause liver injury by an oxygen radical-dependent mechanism. It is unclear whether PMN-derived oxygen radicals, hepatocellular-derived oxygen species resulting from reduced tissue perfusion and reperfusion, or both are involved in the pathogenesis.
Authors:
L J Dahm; A E Schultze; R A Roth
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The American journal of pathology     Volume:  139     ISSN:  0002-9440     ISO Abbreviation:  Am. J. Pathol.     Publication Date:  1991 Nov 
Date Detail:
Created Date:  1991-12-17     Completed Date:  1991-12-17     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  0370502     Medline TA:  Am J Pathol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1009-20     Citation Subset:  AIM; IM    
Affiliation:
Department of Pharmacology and Toxicology, Michigan State University, East Lansing 48824.
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MeSH Terms
Descriptor/Qualifier:
Alanine Transaminase / metabolism
Animals
Catalase / pharmacology
Cell Communication
Cells, Cultured
Free Radicals
Lithocholic Acid / pharmacology
Liver / drug effects,  metabolism,  pathology*
Male
Neutrophils / drug effects,  metabolism,  physiology*
Oxygen / metabolism,  physiology*
Perfusion
Rats
Rats, Inbred Strains
Superoxide Dismutase / pharmacology
Tetradecanoylphorbol Acetate / pharmacology
Grant Support
ID/Acronym/Agency:
ES04139/ES/NIEHS NIH HHS; ES07146/ES/NIEHS NIH HHS
Chemical
Reg. No./Substance:
0/Free Radicals; 16561-29-8/Tetradecanoylphorbol Acetate; 434-13-9/Lithocholic Acid; 7782-44-7/Oxygen; EC 1.11.1.6/Catalase; EC 1.15.1.1/Superoxide Dismutase; EC 2.6.1.2/Alanine Transaminase
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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