| Cardiac UCP2 expression and myocardial oxidative metabolism during acute septic shock in the rat. | |
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MedLine Citation:
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PMID: 12785014 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Septic shock decreases cardiac hydraulic work relative to the rate of myocardial oxygen consumption, causing decreased mechanical efficiency (hydraulic work/myocardial oxygen consumption). This study tested whether the mitochondrial uncoupling protein UCP2 was responsible for decreased cardiac mechanical efficiency after polymicrobial septic shock. Sepsis was initiated in ketamine/xylazine-anesthetized rats by cecal ligation and puncture (CLP). Steady-state mRNA content was quantified by Northern blot analysis, and protein content was estimated by western blot. Additional hearts were removed after 12 h and perfused in working mode to measure work (mmHg x mL/min/100 g dry wt) and efficiency (CE = work/oxygen consumption, %). The 72-h mortality rate was 80%, and deaths occurred between 12-32 h. Cardiac work (152 +/- 15, shock vs. 235 +/- 16, control; P < 0.05) and cardiac efficiency (4.0 +/- 0.4 vs. 5.6 +/- 0.3; P < 0.05) were significantly decreased when hearts were isolated 12 h after CLP. Myocardial UCP2 mRNA expression was increased by 52% (12 h) compared with control hearts; however, there was no detectable UCP2 protein in mitochondria isolated from either control or septic hearts. Conclusions: Although polymicrobial sepsis decreased cardiac mechanical efficiency and increased UCP-2 expression coincident with premortal hypothermia, we did not detect any evidence of UCP-2 protein in septic heart muscle. These data argue against the hypothesis that UCP-2 causes decreased cardiac mechanical efficiency in septic shock. |
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Authors:
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Michael J Roshon; Jeffrey A Kline; Lisa R Thornton; John A Watts |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Shock (Augusta, Ga.) Volume: 19 ISSN: 1073-2322 ISO Abbreviation: Shock Publication Date: 2003 Jun |
Date Detail:
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Created Date: 2003-06-04 Completed Date: 2004-02-24 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 9421564 Medline TA: Shock Country: United States |
Other Details:
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Languages: eng Pagination: 570-6 Citation Subset: IM |
Affiliation:
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Division of Research, Department of Emergency Medicine, Carolinas Medical Center, Charlotte, North Carolina 28323-2861, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acute Disease Animals Base Sequence Cecum / physiology Coronary Circulation / physiology DNA Probes DNA, Complementary Disease Models, Animal Gene Expression Regulation / drug effects Heart / physiopathology* Ion Channels Liver / metabolism Male Membrane Transport Proteins / genetics* Mitochondria, Heart / metabolism* Mitochondrial Proteins / genetics* Muscle, Skeletal / metabolism Myocardium / metabolism* Oxygen Consumption / physiology* Perfusion Peroxidase / metabolism Rats Rats, Sprague-Dawley Shock, Septic / genetics, metabolism*, mortality Survival Analysis |
| Chemical | |
Reg. No./Substance:
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0/DNA Probes; 0/DNA, Complementary; 0/Ion Channels; 0/Membrane Transport Proteins; 0/Mitochondrial Proteins; 0/mitochondrial uncoupling protein 2; EC 1.11.1.7/Peroxidase |
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