| Mechanisms of sepsis-induced cardiac dysfunction. | |
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MedLine Citation:
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PMID: 17452940 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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OBJECTIVES: To review mechanisms underlying sepsis-induced cardiac dysfunction in general and intrinsic myocardial depression in particular. DATA SOURCE: MEDLINE database. DATA SYNTHESIS: Myocardial depression is a well-recognized manifestation of organ dysfunction in sepsis. Due to the lack of a generally accepted definition and the absence of large epidemiologic studies, its frequency is uncertain. Echocardiographic studies suggest that 40% to 50% of patients with prolonged septic shock develop myocardial depression, as defined by a reduced ejection fraction. Sepsis-related changes in circulating volume and vessel tone inevitably affect cardiac performance. Although the coronary circulation during sepsis is maintained or even increased, alterations in the microcirculation are likely. Mitochondrial dysfunction, another feature of sepsis-induced organ dysfunction, will also place the cardiomyocytes at risk of adenosine triphosphate depletion. However, clinical studies have demonstrated that myocardial cell death is rare and that cardiac function is fully reversible in survivors. Hence, functional rather than structural changes seem to be responsible for intrinsic myocardial depression during sepsis. The underlying mechanisms include down-regulation of beta-adrenergic receptors, depressed postreceptor signaling pathways, impaired calcium liberation from the sarcoplasmic reticulum, and impaired electromechanical coupling at the myofibrillar level. Most, if not all, of these changes are regulated by cytokines and nitric oxide. CONCLUSIONS: Integrative studies are needed to distinguish the hierarchy of the various mechanisms underlying septic cardiac dysfunction. As many of these changes are related to severe inflammation and not to infection per se, a better understanding of septic myocardial dysfunction may be usefully extended to other systemic inflammatory conditions encountered in the critically ill. Myocardial depression may be arguably viewed as an adaptive event by reducing energy expenditure in a situation when energy generation is limited, thereby preventing activation of cell death pathways and allowing the potential for full functional recovery. |
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Authors:
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Alain Rudiger; Mervyn Singer |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Review |
Journal Detail:
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Title: Critical care medicine Volume: 35 ISSN: 0090-3493 ISO Abbreviation: Crit. Care Med. Publication Date: 2007 Jun |
Date Detail:
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Created Date: 2007-05-24 Completed Date: 2007-07-02 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0355501 Medline TA: Crit Care Med Country: United States |
Other Details:
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Languages: eng Pagination: 1599-608 Citation Subset: AIM; IM |
Affiliation:
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Bloomsbury Institute of Intensive Care Medicine, Wolfson Institute for Biomedical Research and Department of Medicine, University College London, UK. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Cardiomyopathies / etiology*, metabolism, physiopathology* Cell Death / physiology Energy Metabolism Heart / physiopathology Humans Inflammation / metabolism Microcirculation / physiopathology Mitochondria, Heart / physiology Myocardial Contraction Myocardium / metabolism, pathology Sepsis / complications*, physiopathology* Signal Transduction |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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