Modulation of extracellular atrioventricular node field potential pattern and ventricular rhythm by morphine in experimental atrial fibrillation in isolated rabbit heart

Endorphins are produced by cardiomyocytes, and exert different effects on the heart. The aim of the present study is to assess morphine effects on extracellular atrioventricular (AV) node field potential pattern and ventricular rhythm of isolated rabbit heart during experimental atrial fibrillation (AF). Effects of different concentrations of morphine (10, 20, 50 and 100 μM) were assessed by applying basic stimuli protocols involving Wenckebach, recovery, zone of concealment and concealed conduction parameters during experimental atrial fibrillation in isolated rabbit heart. Two-way ANOVA was used to compare the groups. Morphine significantly suppressed basic parameters of AV node. Morphine (100 μM) significantly increased wenckebach index (153.6±3.9 to 169.8±2.9 ms) and functional refractory period (156.9±3.0 to 176.4±3.5 ms) (P<0.05). During experimental atrial fibrillation, morphine nonsignificantly increased mean His–His interval, concealed conduction and zone of concealment (P > 0.05). The present results showed that morphine has concentration-dependent effects on AV node electrophysiological properties. Morphine at low concentrations can decrease nodal conduction and refractoriness of AV node, but in high concentrations causes increased nodal conduction without concealed conduction changes. Dual effects of morphine can explain the unpredictable behavior of heart in cardiac tachyarrhythmias.