Literature DB >> 14767366

Inactivity and inflammation: selected cytokines as biologic mediators in muscle dysfunction during critical illness.

Chris Winkelman1.   

Abstract

Muscle dysfunction leads to activity intolerance, prolonged hospitalization, and additional days of mechanical ventilation. The etiology of muscle dysfunction in the critically ill patient is multifactoral. Inactivity and inflammation, common phenomena to patients in the intensive care unit, are associated with myopathy and muscle dysfunction. Cytokines are small biological active molecules that regulate inflammation and have a direct effect on muscle wasting. The purpose of this article is to describe selected cytokines (ie, interleukin-1, interleukin-6, interleukin-10, and tumor necrosis factor), explain their role in muscle dysfunction, and explore the role of therapeutic activity as a moderator of muscle dysfunction and cytokine-mediated muscle damage.

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Year:  2004        PMID: 14767366     DOI: 10.1097/00044067-200401000-00006

Source DB:  PubMed          Journal:  AACN Clin Issues        ISSN: 1079-0713


  16 in total

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Review 6.  The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill.

Authors:  O Friedrich; M B Reid; G Van den Berghe; I Vanhorebeek; G Hermans; M M Rich; L Larsson
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7.  Induction of muscle weakness by local inflammation: an experimental animal model.

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Journal:  Inflamm Res       Date:  2009-04       Impact factor: 4.575

8.  TNF signals via neuronal-type nitric oxide synthase and reactive oxygen species to depress specific force of skeletal muscle.

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Journal:  J Appl Physiol (1985)       Date:  2013-04-04

9.  Early rehabilitation in sepsis: a prospective randomised controlled trial investigating functional and physiological outcomes The i-PERFORM Trial (Protocol Article).

Authors:  Geetha Kayambu; Robert J Boots; Jennifer D Paratz
Journal:  BMC Anesthesiol       Date:  2011-10-31       Impact factor: 2.217

10.  Plasma cytokine expression after lower-limb compression in rats.

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Journal:  Rev Bras Ortop       Date:  2014-12-31
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