Increased superoxide production during fatigue in the perfused rat diaphragm

This study test the hypothesis that a temporal relationship exists between the production of superoxide anion (O2-) and the contractile activity of perfused rat diaphragm. O2- levels were determined minute to minute by measuring the reduction of cytochrome c in the perfusate as the diaphragms were s...

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Bibliographic Details
Published in:American journal of respiratory and critical care medicine 1997-07, Vol.156 (1), p.140-145
Main Authors: KOLBECK, R. C, SHE, Z.-W, CALLAHAN, L. A, NOSEK, T. M
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Diaphragm - metabolism
Diaphragm - physiology
Fundamental and applied biological sciences. Psychology
Muscle Contraction - physiology
Muscle Fatigue - physiology
Organ Culture Techniques
Rats
Rats, Sprague-Dawley
Striated muscle. Tendons
Superoxides - metabolism
Vertebrates: osteoarticular system, musculoskeletal system
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Summary:This study test the hypothesis that a temporal relationship exists between the production of superoxide anion (O2-) and the contractile activity of perfused rat diaphragm. O2- levels were determined minute to minute by measuring the reduction of cytochrome c in the perfusate as the diaphragms were subjected to various levels of contractile activity. After equilibrating at low contractile rates (one 500 ms 80 Hz train/min), diaphragms were fatigued by increasing their contractile activity for 5 min (one 500 ms 80 Hz train/s) and then allowed to recover for 30 min (one 500 ms 80 Hz train/min). During equilibration, diaphragms did not produce O2- above the background level measured in the presence of superoxide dismutase (SOD). Within the first minute of fatigue-inducing stimulation, however, the rate of O2- production increased to 0.70 +/- 0.17 nmol/min and remained elevated until the recovery period when production returned towards baseline. SOD blocked this stimulation-related increase of O2-. Tension (+/-SOD) fell to 12% of the control value during the fatigue-inducing stimulation. During recovery the contractile response returned to 51% of control, indicating long-lasting effects on the contractile machinery. SOD did not limit fatigue or improve recovery, probably because it is a large protein that cannot cross cell membranes and protect the cells by scavenging O2- at its site of production.
ISSN:1073-449X
1535-4970
DOI:10.1164/ajrccm.156.1.9610041