| Chronic peritoneal sepsis: myocardial dysfunction, endothelin and signaling mechanisms. | |
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MedLine Citation:
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PMID: 15970572 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Despite advances in the understanding of pathophysiological mechanisms, there are limited pharmacotherapeutic options for sepsis, septic shock, and related pathologies. It is surprising that although sepsis-induced myocardial depression is documented in clinics, the cellular mechanisms are from clear. Alterations in molecular signaling mechanisms activated by cytokines and potent mediators such as ET-1 could pose the risk for myocardial dysfunction in sepsis. Our laboratory data suggest that the septic heart, in vivo, exhibits an increased time constant of left ventricular relaxation, tau, along with changes in LVEDP. We also observed that bigET-1-induced elevation of ET-1 correlates with cardiodynamic alterations, induction of apoptosis, and activation of p38-MAPK phosphorylation during sepsis. In light of these evidences, we emphasize that these molecular alterations in heart, both at organ and cellular level during early sepsis, need to be elucidated thoroughly. |
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Authors:
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Akanksha Gupta; Sachin Brahmbhatt; Ruchita Kapoor; Lisa Loken; Avadhesh C Sharma |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review Date: 2005-09-01 |
Journal Detail:
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Title: Frontiers in bioscience : a journal and virtual library Volume: 10 ISSN: 1093-4715 ISO Abbreviation: Front. Biosci. Publication Date: 2005 |
Date Detail:
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Created Date: 2005-06-22 Completed Date: 2006-09-18 Revised Date: 2011-05-20 |
Medline Journal Info:
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Nlm Unique ID: 9709506 Medline TA: Front Biosci Country: United States |
Other Details:
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Languages: eng Pagination: 3183-205 Citation Subset: IM |
Affiliation:
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Department of Pharmaceutical Sciences, North Dakota State University, Fargo, ND 58105, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apoptosis / physiology Cardiomyopathies / etiology* Cytokines / physiology Endothelins / metabolism* Humans Peritonitis / complications*, metabolism Sepsis / complications Signal Transduction / physiology* |
| Grant Support | |
ID/Acronym/Agency:
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HL066016/HL/NHLBI NIH HHS; R15 HL066016-02/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Cytokines; 0/Endothelins |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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