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Related Experiment Videos

Apocynin improves diaphragmatic function after endotoxin administration.

G Supinski1, D Stofan, D Nethery

  • 1Metrohealth Medical Center, Cleveland 44109, Ohio.

Journal of Applied Physiology (Bethesda, Md. : 1985)
|August 13, 1999
PubMed
Summary
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Free radicals from white blood cells contribute to sepsis-induced diaphragmatic dysfunction. Apocynin, an inhibitor of superoxide production, partially prevented this dysfunction and reduced oxidative stress markers in the diaphragm.

Area of Science:

  • Physiology
  • Pathology
  • Biochemistry

Background:

  • Sepsis can lead to respiratory muscle dysfunction.
  • Neutrophils infiltrate the diaphragm during sepsis.
  • The role of superoxide from white blood cells in sepsis-induced muscle dysfunction is unclear.

Purpose of the Study:

  • To investigate the effect of apocynin, a neutrophil NADPH oxidase inhibitor, on endotoxin-induced diaphragmatic dysfunction.
  • To determine if inhibiting superoxide production can mitigate sepsis-related diaphragm dysfunction.

Main Methods:

  • Rats were administered saline, endotoxin, apocynin, or both.
  • Diaphragm force generation was measured 18 hours post-injection.
  • Diaphragm tissue was analyzed for lipid peroxidation (4-hydroxynonenal) and protein modification (nitrotyrosine).

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Main Results:

  • Endotoxin significantly reduced diaphragm force generation.
  • Apocynin partially preserved diaphragm force in endotoxemic rats.
  • Apocynin inhibited endotoxin-induced increases in 4-hydroxynonenal and nitrotyrosine levels.

Conclusions:

  • Neutrophil-derived free radicals contribute to diaphragmatic dysfunction during sepsis.
  • Inhibiting superoxide production may be a therapeutic strategy for sepsis-induced respiratory muscle weakness.