Characterization of the
Antiarrhythmic Effect of the Trace Element Zinc and its Potential Relationship to
Inhibition of Oxidative Stress
e and others have proposed that the trace element zinc can antagonize copper-and/or
iron- mediated site-specific reactive oxygen intermediate formation, a process thought to
be involved in reperfusion injury. The purpose of this study was further examine the
effect of zinc on reperfusion arrhytmias in an in vitro model of regional ischemia, to
characterize the kinetics of this effect, and to evaluate the potential role of inhibition
of oxidative stress. Rat hearts were perfused in the Langendorff mode with a standard
Krebs-Henseleit buffer. Hearts, perfused with buffer containing increasing concentrations
of zinc-bis-histidinate, showed decreased incidence and duration of ventricular
fibrillation. A pharmacokinetic profile was determined by altering the preischemic loading
period. Hearts were perfused with 20 mcM zinc for up to 20 min. preischemic or perfused
with zinc during the ischemic and reperfusion periods alone. As the duration of the
preiscxhemic zinc load increased there was a significant decrease in the incidence and
duration of VF, and a concomitant increase in incidence and duration of NSR. Pacing
experiments were conducted to account for the negative chronotropic effect of zinc. Using
salicylate as a free radical probe, it was determined that preischemic perfusion with 20
mcM zinc decreased background 'OH formation after regional ischemia. These results
demonstrate that zinc decreases reperfusion injury, possibly through a mechanism involving
decreased formation of reactive oxygen intermediates. LT Aiuto, SR Powell, J Trace Elem
Exp Med 1995;8:173-182.
Copyright © 2003 Anamol Laboratories Ltd.
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