Erythrocytes decrease myocardial hydrogen peroxide levels and reperfusion injury

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

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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)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume256
Issue number2
Publication statusPublished - 1989
Externally publishedYes

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ASJC Scopus subject areas

  • Physiology

Cite this

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