FJ McNicol
Skeletal muscle contractile properties and proinflammatory cytokine gene expression in human endotoxaemia
McNicol, FJ; Hoyland, JA; Cooper, RG; Carlson, GL
Authors
JA Hoyland
RG Cooper
GL Carlson
Abstract
Background: Muscle dysfunction associated with sepsis contributes to morbidity and mortality but
the underlying mechanisms are unclear. This study examined whether muscle weakness relates to an
intrinsic defect in contraction, or to central mechanisms associated with acute illness, and whether
systemic endotoxaemia induces changes in gene expression for proinflammatory cytokines within human
muscle in vivo.
Methods: In this experimental study, 12 healthy men received intravenous Escherichia coli
lipopolysaccharide (LPS, 4 ng/kg) or saline (control). Voluntary and electrically stimulated quadriceps
contraction, and tumour necrosis factor (TNF) α mRNA expression in quadriceps muscle biopsies were
studied before and after the infusion.
Results: Endotoxaemia induced transient weakness of voluntary quadriceps contraction, equivalent to
a 7·8 (95 per cent confidence interval 2·1 to 13·5) per cent reduction in contractile force at 180 min
(P = 0·027) and a 9·0 (5·2 to 12·8) per cent reduction at 300 min (P = 0·008). Electrically stimulated
contraction was unaffected. LPS administration resulted in an apparent fibre-specific induction of TNF-α
mRNA.
Conclusion: Endotoxaemia results in a reduction in voluntary muscle contractile force without an
apparent defect in stimulated muscle contraction. Loss of volition may be a more important factor than
intrinsic dysfunction in acute sepsis-associated human muscle weakness.
Citation
McNicol, F., Hoyland, J., Cooper, R., & Carlson, G. (2010). Skeletal muscle contractile properties and proinflammatory cytokine gene expression in human endotoxaemia. British Journal of Surgery, 97(3), 434-442. https://doi.org/10.1002/bjs.6868
Journal Article Type | Article |
---|---|
Publication Date | Jan 1, 2010 |
Deposit Date | Sep 11, 2014 |
Journal | British Journal of Surgery |
Print ISSN | 0007-1323 |
Publisher | Wiley |
Peer Reviewed | Peer Reviewed |
Volume | 97 |
Issue | 3 |
Pages | 434-442 |
DOI | https://doi.org/10.1002/bjs.6868 |
Publisher URL | http://dx.doi.org/10.1002/bjs.6868 |
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