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Effects of hyperoxia on rat diaphragm function

A Anzueto1, J M Brassard, F H Andrade

  • 1Department of Medicine, University of Texas Health Science Center at San Antonio.

Journal of Applied Physiology (Bethesda, Md. : 1985)
|July 1, 1994
PubMed
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Prolonged exposure to high oxygen levels impairs diaphragm function in rats by increasing oxidative stress. This oxygen-induced diaphragm dysfunction is worsened by inspiratory resistive loading, highlighting the role of free radicals.

Area of Science:

  • Physiology
  • Biochemistry
  • Respiratory Medicine

Background:

  • Inspiratory resistive loading (IRL) is associated with oxygen radical generation and impaired diaphragm performance.
  • Normobaric hyperoxia (O2) may induce diaphragm dysfunction via free radical production.

Purpose of the Study:

  • To investigate the effects of normobaric hyperoxia on diaphragm function in rats.
  • To determine if hyperoxia-induced free radical production impairs diaphragm contractile properties.

Main Methods:

  • Sprague-Dawley rats were exposed to >95% O2 for 24, 48, or 60 hours.
  • Diaphragm function was assessed at rest and after inspiratory resistive loading.
  • Glutathione (GSH, GSSG) concentrations and contractile properties (Po, Pt) were measured.

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Main Results:

  • Hyperoxia >48 hours significantly decreased maximal tetanic tension (Po) and maximal twitch tension (Pt).
  • Increased GSSG content and GSSG-to-GSH ratios indicated oxidative stress.
  • IRL further reduced Po and Pt in hyperoxia-exposed animals.

Conclusions:

  • Hyperoxia exposure, particularly >48 hours, impairs diaphragm function in rats.
  • Free radical generation likely contributes to hyperoxia-induced diaphragm dysfunction.
  • The glutathione redox cycle is activated, suggesting a cellular response to oxidative stress.