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      Propofol Inhibits Lipopolysaccharide-Induced Tumor Necrosis Factor-Alpha Expression and Myocardial Depression through Decreasing the Generation of Superoxide Anion in Cardiomyocytes

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          Abstract

          TNF- α has been shown to be a major factor responsible for myocardial depression in sepsis. The aim of this study was to investigate the effect of an anesthetic, propofol, on TNF- α expression in cardiomyocytes treated with LPS both in vivo and in vitro. In cultured cardiomyocytes, compared with control group, propofol significantly reduced protein expression of gp91phox and phosphorylation of extracellular regulated protein kinases 1/2 (ERK1/2) and p38 MAPK, which associates with reduced TNF- α production. In in vivo mice studies, propofol significantly improved myocardial depression and increased survival rate of mice after LPS treatment or during endotoxemia, which associates with reduced myocardial TNF- α production, gp91phox, ERK1/2, and p38 MAPK. It is concluded that propofol abrogates LPS-induced TNF- α production and alleviates cardiac depression through gp91phox/ERK1/2 or p38 MAPK signal pathway. These findings have great clinical importance in the application of propofol for patients enduring sepsis.

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          Most cited references36

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          NADPH oxidase-dependent signaling in endothelial cells: role in physiology and pathophysiology.

          Reactive oxygen species (ROS) including superoxide (O(2)(.-)) and hydrogen peroxide (H(2)O(2)) are produced endogenously in response to cytokines, growth factors; G-protein coupled receptors, and shear stress in endothelial cells (ECs). ROS function as signaling molecules to mediate various biological responses such as gene expression, cell proliferation, migration, angiogenesis, apoptosis, and senescence in ECs. Signal transduction activated by ROS, "oxidant signaling," has received intense investigation. Excess amount of ROS contribute to various pathophysiologies, including endothelial dysfunction, atherosclerosis, hypertension, diabetes, and acute respiratory distress syndrome (ARDS). The major source of ROS in EC is a NADPH oxidase. The prototype phagaocytic NADPH oxidase is composed of membrane-bound gp91phox and p22hox, as well as cytosolic subunits such as p47(phox), p67(phox) and small GTPase Rac. In ECs, in addition to all the components of phagocytic NADPH oxidases, homologues of gp91(phox) (Nox2) including Nox1, Nox4, and Nox5 are expressed. The aim of this review is to provide an overview of the emerging area of ROS derived from NADPH oxidase and oxidant signaling in ECs linked to physiological and pathophysiological functions. Understanding these mechanisms may provide insight into the NADPH oxidase and oxidant signaling components as potential therapeutic targets.
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            Atrial fibrillation among Medicare beneficiaries hospitalized with sepsis: incidence and risk factors.

            Newly diagnosed atrial fibrillation (AF) during severe sepsis is associated with increased risks of in-hospital stroke and mortality. However, the prevalence, incidence, and risk factors associated with AF during the sepsis syndromes are unclear. We identified patients with preexisting, newly diagnosed, or no AF in a nationally representative 5% sample of Medicare beneficiaries hospitalized with sepsis between 2004 and 2007. We identified multivariable-adjusted demographic and clinical characteristics associated with development of newly diagnosed AF during a sepsis hospitalization. A total of 60,209 beneficiaries had a sepsis hospitalization. Mean age was 80.2 years, 44.4% were men, and 83.1% were white. Atrial fibrillation occurred during 25.5% (95% CI 25.2-25.9) of sepsis hospitalizations, including 18.3% (18.0%-18.7%) with preexisting AF and 7.2% (7.0%-7.4%) with newly diagnosed AF. Patients with sepsis requiring intensive care had a greater risk of newly diagnosed AF (10.7%, 95% CI 10.3%-11.1%) compared with patients who did not require intensive care (4.4%, 4.2%-4.5%, P < .001). In multivariable analysis, factors associated with newly diagnosed AF during sepsis included older age, white race, acute organ dysfunction, intensive care unit admission, mechanical ventilation, right heart catheterization, diagnosis of endocarditis, and coronary artery bypass graft surgery. Cardiovascular comorbid conditions generally were not associated with increased risk for newly diagnosed AF during sepsis. Atrial fibrillation is common among critically ill patients with sepsis. Acute factors, rather than preexisting cardiovascular comorbid conditions, are associated with increased risk for newly diagnosed AF during sepsis, suggesting that mechanisms of newly diagnosed AF during sepsis may differ from the general population of patients with AF. Copyright © 2013 Mosby, Inc. All rights reserved.
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              New approaches to the study of sepsis

              Peter Ward (2012)
              Models of sepsis have been instructive in understanding the sequence of events in animals and, to an extent, in humans with sepsis. Events developing early in sepsis suggest that a hyperinflammatory state exists, accompanied by a buildup of oxidants in tissues reflective of a redox imbalance. Development of immunosuppression and degraded innate and adaptive immune responses are well-established complications of sepsis. In addition, there is robust activation of the complement system, which contributes to the harmful effects of sepsis. These events appear to be associated with development of multiorgan failure. The relevance of animal models of sepsis to human sepsis and the failure of human clinical trials are discussed, together with suggestions as to how clinical trial design might be improved.
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                Author and article information

                Journal
                Oxid Med Cell Longev
                Oxid Med Cell Longev
                OMCL
                Oxidative Medicine and Cellular Longevity
                Hindawi Publishing Corporation
                1942-0900
                1942-0994
                2014
                11 August 2014
                : 2014
                : 157376
                Affiliations
                1Department of Anesthesiology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China
                2Department of Orthopedics and Traumatology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China
                3Department of Anesthesiology, The University of Hongkong Shenzhen Hospital, Shenzhen, Guangdong 518053, China
                Author notes
                *You-Tan Liu: liuyt@ 123456hku-szh.org and
                *Zai-Sheng Qin: mzqinzs@ 123456126.com

                Academic Editor: Neelam Khaper

                Article
                10.1155/2014/157376
                4144395
                25180066
                09431282-a0f4-441c-b8fd-249acee39f8f
                Copyright © 2014 Jing Tang et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 18 April 2014
                : 16 July 2014
                Categories
                Research Article

                Molecular medicine
                Molecular medicine

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