Erythrocytes decrease myocardial hydrogen peroxide levels and reperfusion injury

J. M. Brown, M. A. Grosso, L. S. Terada, C. J. Beehler, K. M. Toth, G. J. Whitman, A. H. Harken, J. E. Repine

Research output: Contribution to journalArticle

47 Scopus citations

Abstract

Reperfusion with untreated, carbon monoxide-treated, or glutaraldehyde-fixed human erythrocytes (RBC) increased ventricular function and decreased myocardial hydrogen peroxide (H2O2) levels [assessed by H2O2-dependent aminotriazole (AMT) inactivation of myocardial catalase activities] of ischemic, isolated rat hearts. In contrast, reperfusion with RBC that lacked catalase (AMT treated) and/or glutathione (N-ethylmaleimide treated) did not increase ventricular function or decrease myocardial H2O2 levels as much as reperfusion with untreated RBC. By comparison, reperfusion with superoxide dismutase-depleted (diethyldithiocarbamate-treated) or anion channel-inhibited (diisothiocyanodisulfonic acid stilbene-treated) RBC increased ventricular function and decreased myocardial H2O2 levels the same as untreated RBC. The results suggest that catalase and/or glutathione in intact RBC can decrease endogenously generated H2O2 and related reperfusion injury in ischemic, isolated perfused hearts.

Original languageEnglish (US)
Pages (from-to)25/2
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume256
Issue number2
StatePublished - Jan 1 1989

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

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    Brown, J. M., Grosso, M. A., Terada, L. S., Beehler, C. J., Toth, K. M., Whitman, G. J., Harken, A. H., & Repine, J. E. (1989). Erythrocytes decrease myocardial hydrogen peroxide levels and reperfusion injury. American Journal of Physiology - Heart and Circulatory Physiology, 256(2), 25/2.