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Dexrazoxane Prevents Myocardial Ischemia/Reperfusion-Induced Oxidative Stress in the Rat Heart

  • Basic Pharmacology
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Abstract

Introduction

Dexrazoxane (Dex), used clinically to protect against anthracycline-induced cardiotoxicity, possesses iron-chelating properties. The present study was designed to examine whether Dex could inhibit the ischemia/reperfusion (I/R) induced damage to the rat heart.

Materials and methods

Isolated perfused rat hearts were exposed to global ischemia (37°C) and 60 min reperfusion. Dex was perfused for 10 min prior to the ischemia, or administered intraperitoneally (150 mg) 30 min prior to anesthesia of the rats. I/R caused a significant hemodynamic function decline in control hearts during the reperfusion (e.g., the work index LVDP X HR declined to 42.7±10%). Dex (200 μM) applied during the preischemia significantly increased the hemodynamic recovery following reperfusion (LVDP X HR recovered to 55.7±8.8%, p<0.05 vs. control). Intraperitoneal Dex, too, significantly increased the hemodynamic recovery of the reperfused hearts. I/R caused an increase in oxidation of cytosolic proteins, while Dex decreased this oxidation.

Discussion

The decrease in proteins carbonylation and correlative hemodynamic improvement suggests that Dex decreases I/R free radical formation and reperfusion injury.

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Correspondence to Herzl Schwalb.

Additional information

Eyal Ramu and Amit Korach contributed equally to this study.

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Ramu, E., Korach, A., Houminer, E. et al. Dexrazoxane Prevents Myocardial Ischemia/Reperfusion-Induced Oxidative Stress in the Rat Heart. Cardiovasc Drugs Ther 20, 343–348 (2006). https://doi.org/10.1007/s10557-006-0497-4

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  • DOI: https://doi.org/10.1007/s10557-006-0497-4

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