Document Detail


Neutrophil activation as a mechanism of tissue injury.
MedLine Citation:
PMID:  6623096     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
C5A is capable of causing granulocyte/granulocyte interactions that lead to clumping, vasoocclusion, and the extension of infarctive damage in patients with coronary artery disease. Employing a new rheologic procedure, laser transillumination of thin vascular beds, one directly observes in vivo granulocyte aggregation in the mesentery of the rat. Nonsteroidal antiinflammatory drugs (NSAIDs) were shown to stop granulocyte agglomeration and to limit the extension of experimental myocardial infarcts in the cat. There may be application for NSAIDs for myocardial infarction in humans. NSAIDs block granulocyte aggregation to both a traditional activated complement and a complement activated by cryoglobulins. Patients with severe cryoglobulinemic cutaneous vasculitis who failed on steroids responded to NSAID administration.
Authors:
H S Jacob
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Seminars in arthritis and rheumatism     Volume:  13     ISSN:  0049-0172     ISO Abbreviation:  Semin. Arthritis Rheum.     Publication Date:  1983 Aug 
Date Detail:
Created Date:  1983-11-23     Completed Date:  1983-11-23     Revised Date:  2005-11-17    
Medline Journal Info:
Nlm Unique ID:  1306053     Medline TA:  Semin Arthritis Rheum     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  144-7     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Anti-Inflammatory Agents / therapeutic use*
Cats
Cell Aggregation / drug effects
Complement Activation*
Complement C5 / immunology
Complement C5a
Cryoglobulins / immunology
Humans
Myocardial Infarction / drug therapy,  immunology
Neutrophils / immunology*
Rats
Vasculitis / drug therapy,  immunology*
Chemical
Reg. No./Substance:
0/Anti-Inflammatory Agents; 0/Complement C5; 0/Cryoglobulins; 80295-54-1/Complement C5a

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


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