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Monocyte inflammatory mediators impair in vitro hamster diaphragm contractility
P Wilcox1, S Osborne, B Bressler
1Department of Medicine, University of British Columbia, Vancouver, Canada.
The American Review of Respiratory Disease
|August 1, 1992
Summary
Sepsis impairs diaphragm function. Inflammatory mediators from monocytes directly reduce muscle contractility, affecting respiratory strength.
Area of Science:
- Physiology
- Immunology
- Respiratory Medicine
Background:
- Sepsis is known to cause ventilatory muscle dysfunction.
- The direct impact of inflammatory mediators on muscle fibers in sepsis is not fully understood.
Purpose of the Study:
- To investigate if inflammatory mediators from monocytes directly affect diaphragm muscle fiber contractility in vitro.
- To determine the impact of lipopolysaccharide-stimulated monocyte supernatant on diaphragm function.
Main Methods:
- In vitro studies on hamster costal diaphragm preparations.
- Measurement of baseline contractility (peak twitch, tetanic tension, relaxation time, time-to-peak tension, force-frequency response) and fatigability.
- Incubation of diaphragm preparations with Krebs solution, nonstimulated monocyte supernatant, or lipopolysaccharide-stimulated monocyte supernatant.
Main Results:
- Lipopolysaccharide-stimulated monocyte supernatant significantly reduced peak twitch and tetanic tension in diaphragm preparations.
- A faster relaxation time and a rightward shift in the force-frequency response were observed in the stimulated group.
- No significant changes in contractility or fatigue were noted in control or nonstimulated supernatant groups.
Conclusions:
- Monocyte secretory products, particularly those released upon lipopolysaccharide stimulation, directly impair diaphragmatic contractility.
- These findings suggest a direct mechanism by which sepsis-induced inflammation affects respiratory muscle function.