Effect of superoxide dismutase and catalase on regional dysfunction after exercise-induced ischemia

D. C. Homans, R. Asinger, T. Pavek, M. Crampton, P. Lindstrom, Douglas A Peterson, R. J. Bache

Research output: Contribution to journalArticlepeer-review

14 Scopus citations

Abstract

This study was designed to test the hypothesis that the oxygen free radical scavengers superoxide dismutase (SOD) and catalase may reduce myocardial 'stunning' after exercise-induced ischemia. To test this hypothesis, 8 mongrel dogs performed treadmill exercise for 10 min in the presence of a flow-limiting coronary artery stenosis. Regional left ventricular function was measured with ultrasonic microcrystals implanted to measure regional wall thickening. Regional myocardial perfusion was measured with radioactive microspheres. The combination of SOD (5 mg/kg iv) and catalase (5 mg/kg iv) did not affect heart rate, blood pressure, coronary artery flow, or regional myocardial blood flow at rest, during exercise, or in the postexercise period. SOD and catalase had no effect on regional wall thickening at rest before exercise. During exercise in the absence of a coronary artery stenosis, thickening was slightly lower during SOD and catalase infusion (27 ± 11.0 vs. 30.8 ± 11.5%, SOD vs. control P = 0.05). During exercise in the presence of a coronary artery stenosis, there was no difference in thickening. Infusion of SOD and catalase affected neither the transient rebound function occurring early after exercise nor the prolonged period of stunning. These results indicate that the myocardial stunning that follows exercise-induced ischemia is unlikely to be mediated by oxygen free radicals.

Original languageEnglish (US)
Pages (from-to)H392-H398
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume263
Issue number2 32-2
DOIs
StatePublished - 1992

Keywords

  • exercise
  • free radicals
  • myocardial ischemia

Fingerprint Dive into the research topics of 'Effect of superoxide dismutase and catalase on regional dysfunction after exercise-induced ischemia'. Together they form a unique fingerprint.

Cite this