Effects of hyperoxia on rat diaphragm function

A. Anzueto, J. M. Brassard, F. H. Andrade, R. A. Lawrence, L. C. Maxwell, S. M. Levine, S. G. Jenkinson

Research output: Contribution to journalArticlepeer-review

10 Scopus citations


The association of oxygen radical generation with impaired diaphragm performance has previously been reported after inspiratory resistive loading (IRL). We hypothesized that exposure of rats to normobaric hyperoxia (O2) could produce impaired diaphragm function because of free radical production. Sprague-Dawley rats were divided into four groups: 1) room air (control), 2) >95% O2 for 24 h, 3) >95% O2 for 48 h, and 4) >95% O2 for 60 h. Each group was studied at rest after the O2 exposure and then after IRL. During IRL, the animals breathed through an inspiratory resistor until they were unable to sustain >70% of the maximum airway pressure. Diaphragm samples were obtained for analysis of glutathione (GSH) and glutathione disulfide (GSSG) concentrations. In vitro isometric contractile properties were also determined, including maximal tetanic tension (P(o)) and maximal twitch tension (P(t)), in GSSG content and in GSSG-to-GSH ratios. Hyperoxia for >48 h resulted in significant decreases in P(o) and P(t) and an increase in GSSG content and in GSSG-to-GSH ratios compared with other groups. Those same animals subjected to IRL showed a further decrease in P(o) and P(t). These data suggest that free radical generation may occur in the diaphragm during a hyperoxia exposure associated with activation of the GSH redox cycle and impairment of diaphragm function.

Original languageEnglish (US)
Pages (from-to)63-68
Number of pages6
JournalJournal of applied physiology
Issue number1
StatePublished - 1994


  • contractile properties
  • fatigue
  • free radicals
  • glutathione
  • resistive breathing
  • respiratory muscles

ASJC Scopus subject areas

  • Physiology (medical)
  • Physiology


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