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Updated: Jul 14, 2026
14:02
Ex Vivo Assessment of Contractility, Fatigability and Alternans in Isolated Skeletal Muscles
Published on: November 1, 2012
Temporal correlation between maximum tetanic force and cell death in postischemic rat skeletal muscle
H Suzuki1, D C Poole, B W Zweifach
1Department of Bioengineering, Institute for Biomedical Engineering, University of California San Diego, La Jolla, 92093-0412, USA.
The Journal of Clinical Investigation
|December 1, 1995
Summary
Muscle dysfunction after ischemia-reperfusion is linked to cell death, likely caused by oxygen radicals. Interventions reducing these radicals improved muscle force and reduced cell death.
Area of Science:
- Physiology
- Cell Biology
- Biochemistry
Background:
- Ischemia-reperfusion injury (IRI) is a significant clinical problem.
- Muscle dysfunction following IRI is not fully understood.
- Oxygen radicals are implicated in IRI.
Purpose of the Study:
- To investigate the mechanisms of muscle dysfunction after ischemia-reperfusion.
- To correlate cell death with force production.
- To assess the role of oxygen radicals in IRI.
Main Methods:
- Developed a rat spinotrapezius muscle preparation for in vivo measurements.
- Measured maximum tetanic force production.
- Assessed cell death using propidium iodide (PI) staining and mitochondrial membrane potential (deltapsi) via Rhodamine 123 fluorescence.
Main Results:
- Ischemia-reperfusion significantly reduced maximum tetanic force and increased PI-positive myocyte nuclei.
- Oxygen radical scavengers (dimethylthiourea, superoxide dismutase) attenuated force loss and PI staining.
- Low initial mitochondrial membrane potential correlated with greater myocyte injury.
Conclusions:
- Myocyte injury, indicated by PI staining, correlates with impaired contractile function after IRI.
- Oxygen radicals likely mediate myocyte injury and subsequent muscle dysfunction.
- Mitochondrial oxidative potential is a key factor in myocyte susceptibility to IRI.
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