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 cytokinemediated muscle damage.
Biological Mediators| January 01 2004
Inactivity and Inflammation: Selected Cytokines as Biologic Mediators in Muscle Dysfunction During Critical Illness
Chris Winkelman, PhD, RN, CCRN
From Case Western Reserve University, Frances Payne Bolton School of Nursing, Cleveland, Ohio.
Reprint requests to: Chris Winkelman, PhD, RN, CCRN, Assistant Professor, Case Western Reserve University, Frances Payne Bolton School of Nursing, Cleveland, OH (firstname.lastname@example.org).
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AACN Adv Crit Care (2004) 15 (1): 74-82.
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Chris Winkelman; Inactivity and Inflammation: Selected Cytokines as Biologic Mediators in Muscle Dysfunction During Critical Illness. AACN Adv Crit Care 1 January 2004; 15 (1): 74–82. doi: https://doi.org/
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