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This investigation was to examine the effect of ferrous ion (a prooxidant) on the antiarrhythmic effect of naloxone (an endogenous opioid receptor antagonist) in isolated rat hearts. Isolated Sprague-Dawley rat hearts were perfused in the Langendorff mode and myocardial ischemia was performed by ligating the left descending coronary artery. Cardiac rhythm was recorded. Heart alpha-tocopherol concentrations were analyzed. Naloxone (1.2 micromol/heart) was effective in reducing the severity of arrhythmia (arrhythmia score; mean+/-S.E.M: 2.82+/-0.69 for naloxone vs. 5.18+/-0.38 for control, p&lt;0.01). Fe2+ (100 nmol/heart) alone did not significantly affect the arrhythmia score (5.63+/-0.32) when compared with the control, however, Fe2+ administration did cause significant early onset of ventricular premature contraction and ventricular tachycardia. Additionally, Fe2+ administration diminished the naloxone's antiarrhythmic effect (arrhythmia score 4.12+/-0.40). Alpha-tocopherol, a major free radical scavenger that exerts protective functions on heart tissues during myocardial ischemia/reperfusion, was significantly higher in the naloxone-treated group (59.05+/-3.00 nmol/g wet wt) than in the control group (43.84+/-4.17 nmol/g wet wt, p&lt;0.05). These results suggest that endogenous opioid peptides and reactive oxygen species might be related to ischemia-induced arrhythmia.

Ferrous Ion Diminshed the Antiarrhythmic Effect of Naloxone in Myocardial Ischemia of Isolated Rat Hearts.