1998 年 21 巻 7 号 p. 710-712
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 α-tocopherol concentrations were analyzed. Naloxone (1, 2 μmol/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<0.01). Fe2+ (100nmol/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). α-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<0.05). These results suggest that endogenous opioid peptides and reactive oxygen species might be related to ischemia-induced arrhythmia.
