The coincidence of myocardial reperfusion injury and hydrogen perioxide production in the isolated rat heart

J. M. Brown, M. A. Grosso, G. J. Whitman, A. Banerjee, L. S. Terada, J. E. Repine, A. H. Harken

Research output: Contribution to journalArticle

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Abstract

To investigate the specific nature and timing of oxygen (O2) metabolite reperfusion injury, we used a rat-heart model (Langendorff's solution, 37° C) and hydrogen peroxide (H2O2)-dependent aminotriazole inactivation of catalase as a measure of myocardial H2O2 before, during, and after ischemia. We found that after ischemia (20 minutes, global, 37° C), ventricular functional loss - as assessed by measurement of developed pressure (DP), +dp/dt, and -dp/dt with a ventricular balloon - occurred at 10 minutes of reperfusion and that myocardial H2O2 production was maximal by this time. Furthermore, H2O2 production did not occur during ischemia, and inhibition of xanthine oxidase by tungsten feeding or infusing a permeable O2 metabolite scavenger during reperfusion (dimethylthiourea) prevented ventricular functional loss. We conclude that (1) reperfusion injury is in part mediated by toxic oxygen metabolites, (2) H2O2 is the central O2 metabolite responsible for reperfusion injury, and (3) the timing of H2O2 production coincides with the timing of ventricular functional loss.

Original languageEnglish (US)
Pages (from-to)496-501
Number of pages6
JournalSurgery
Volume105
Issue number4
StatePublished - 1989

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Myocardial Reperfusion Injury
Reperfusion Injury
Hydrogen
Ischemia
Amitrole
Oxygen
Myocardial Reperfusion
Tungsten
Xanthine Oxidase
Poisons
Catalase
Hydrogen Peroxide
Reperfusion
Pressure

ASJC Scopus subject areas

  • Surgery

Cite this

Brown, J. M., Grosso, M. A., Whitman, G. J., Banerjee, A., Terada, L. S., Repine, J. E., & Harken, A. H. (1989). The coincidence of myocardial reperfusion injury and hydrogen perioxide production in the isolated rat heart. Surgery, 105(4), 496-501.

The coincidence of myocardial reperfusion injury and hydrogen perioxide production in the isolated rat heart. / Brown, J. M.; Grosso, M. A.; Whitman, G. J.; Banerjee, A.; Terada, L. S.; Repine, J. E.; Harken, A. H.

In: Surgery, Vol. 105, No. 4, 1989, p. 496-501.

Research output: Contribution to journalArticle

Brown, JM, Grosso, MA, Whitman, GJ, Banerjee, A, Terada, LS, Repine, JE & Harken, AH 1989, 'The coincidence of myocardial reperfusion injury and hydrogen perioxide production in the isolated rat heart', Surgery, vol. 105, no. 4, pp. 496-501.
Brown JM, Grosso MA, Whitman GJ, Banerjee A, Terada LS, Repine JE et al. The coincidence of myocardial reperfusion injury and hydrogen perioxide production in the isolated rat heart. Surgery. 1989;105(4):496-501.
Brown, J. M. ; Grosso, M. A. ; Whitman, G. J. ; Banerjee, A. ; Terada, L. S. ; Repine, J. E. ; Harken, A. H. / The coincidence of myocardial reperfusion injury and hydrogen perioxide production in the isolated rat heart. In: Surgery. 1989 ; Vol. 105, No. 4. pp. 496-501.
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AU - Grosso, M. A.

AU - Whitman, G. J.

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AU - Terada, L. S.

AU - Repine, J. E.

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AB - To investigate the specific nature and timing of oxygen (O2) metabolite reperfusion injury, we used a rat-heart model (Langendorff's solution, 37° C) and hydrogen peroxide (H2O2)-dependent aminotriazole inactivation of catalase as a measure of myocardial H2O2 before, during, and after ischemia. We found that after ischemia (20 minutes, global, 37° C), ventricular functional loss - as assessed by measurement of developed pressure (DP), +dp/dt, and -dp/dt with a ventricular balloon - occurred at 10 minutes of reperfusion and that myocardial H2O2 production was maximal by this time. Furthermore, H2O2 production did not occur during ischemia, and inhibition of xanthine oxidase by tungsten feeding or infusing a permeable O2 metabolite scavenger during reperfusion (dimethylthiourea) prevented ventricular functional loss. We conclude that (1) reperfusion injury is in part mediated by toxic oxygen metabolites, (2) H2O2 is the central O2 metabolite responsible for reperfusion injury, and (3) the timing of H2O2 production coincides with the timing of ventricular functional loss.

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