| Lysozyme: a mediator of myocardial depression and adrenergic dysfunction in septic shock in dogs. | |
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MedLine Citation:
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PMID: 12676541 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The objective of the present study was to identify the nature of a filterable cardiodepressant substance (FCS) that contributes to myocardial dysfunction in a canine model of Escherichia coli septic shock. In a previous study, it was found that FCS increased in plasma after 4 h of bacteremia (Am J Physiol 1993;264:H1402) in which FCS was identified by a bioassay that included a right ventricular trabecular (RVT) preparation. In that study, FCS was only partially identified by pore filtration techniques and was found to be a protein of molecular weight between 10 and 30 K. In the present study, FCS was further purified by size exclusion high-pressure liquid chromatography, until a single band was identified on one-dimensional gel electrophoresis. This band was then subjected to tandem mass spectrometry and protein-sequencing techniques and both techniques identified FCS as lysozyme c (Lzm-S), consistent with that originating from the canine spleen. Confirmatory tests showed that purified Lzm-S produced myocardial depression in the RVT preparation at concentrations achieved during sepsis in the in vivo preparation. In addition, Lzm-S inhibited the adrenergic response induced by field stimulation and the beta- agonist isoproterenol in in vitro preparations, these results suggesting that Lzm-S may inhibit the sympathetic response in sepsis. The present findings indicate that Lzm-S originating from disintegrating leukocytes from organs such as the spleen contributes to myocardial dysfunction in this model. The mechanism may relate to its binding or hydrolysis of a cardiac membrane glycoprotein thereby interfering with myocardial excitation-contraction coupling in sepsis. |
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Authors:
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Steven N Mink; Hans Jacobs; Deepak Bose; Krika Duke; Zhao Qin Cheng; Gang Liu; R Bruce Light |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Journal of molecular and cellular cardiology Volume: 35 ISSN: 0022-2828 ISO Abbreviation: J. Mol. Cell. Cardiol. Publication Date: 2003 Mar |
Date Detail:
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Created Date: 2003-04-04 Completed Date: 2003-12-29 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 0262322 Medline TA: J Mol Cell Cardiol Country: England |
Other Details:
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Languages: eng Pagination: 265-75 Citation Subset: IM |
Affiliation:
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Department of Medicine, University of Manitoba, Manitoba R3E-0Z3, Winnipeg, Canada. minksn@cc.umanitoba.ca |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adrenergic Antagonists
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isolation & purification,
toxicity* Adrenergic beta-Agonists / pharmacology Animals Dogs Escherichia coli Infections / chemically induced, etiology*, physiopathology Heart / physiopathology* Isometric Contraction Isoproterenol / pharmacology Muramidase / isolation & purification, toxicity* Myocardial Contraction / drug effects Shock, Septic / chemically induced, etiology*, physiopathology Spleen / enzymology Trisaccharides / pharmacology |
| Chemical | |
Reg. No./Substance:
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0/Adrenergic Antagonists; 0/Adrenergic beta-Agonists; 0/Trisaccharides; 41708-93-4/chitotriose; 7683-59-2/Isoproterenol; EC 3.2.1.17/Muramidase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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