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N-acetylcysteine administration and loaded breathing
G S Supinski1, D Stofan, R Ciufo
1Department of Medicine, Case Western Reserve University, Cleveland, Ohio, USA.
Journal of Applied Physiology (Bethesda, Md. : 1985)
|July 1, 1995
Summary
N-acetylcysteine (NAC) supplementation did not prevent respiratory failure during loaded breathing in rats. While NAC preserved diaphragmatic glutathione levels and reduced muscle fatigue, it did not alter the time to respiratory arrest.
Area of Science:
- Physiology
- Biochemistry
- Respiratory Medicine
Background:
- Loaded breathing alters diaphragmatic glutathione metabolism.
- Glutathione depletion may contribute to respiratory muscle fatigue and failure.
Purpose of the Study:
- To investigate if N-acetylcysteine (NAC) can increase diaphragmatic glutathione and delay respiratory failure during loaded breathing.
- To assess the impact of NAC on diaphragmatic contractility and fatigue.
Main Methods:
- Decerebrate, unanesthetized rats underwent massive inspiratory loading until respiratory arrest.
- Groups received either saline or NAC.
- Diaphragmatic glutathione levels (GSH, GSSG) and in vitro contractility were measured post-arrest.
Main Results:
- Loaded breathing reduced diaphragmatic GSH, increased GSSG, and impaired contractility in saline-treated rats.
- NAC blunted GSH depletion and reduced in vitro diaphragm fatigability.
- NAC did not significantly alter time to respiratory arrest or the force-frequency relationship.
Conclusions:
- Free radical-mediated glutathione depletion is likely not the primary factor causing respiratory failure in this loaded breathing model.
- NAC may mitigate some aspects of diaphragm dysfunction but does not prevent respiratory arrest under severe load.