AIMS: We evaluated the effect of carvedilol, a beta-blocker with anti-oxidative action, against the atrial fibrillation (AF) inducibility, the development of atrial remodeling and the oxidative stress markers in a canine AF model. METHODS AND RESULTS: AF model was produced by performing 6-week rapid atrial stimulation in 15 dogs. The animals were divided into the following three groups: (I) pacing + carvedilol group (n=5); (II) pacing control group (n=5); and (III) non-pacing group (n=5). AF inducibility was gradually increased along the time course in the pacing control group. In the pacing + carvedilol group, the AF inducibility was suppressed especially in the latter phase of protocol in comparison with the pacing control group. Although carvedilol has beta-blocking effect, pacing control and pacing + carvedilol groups did not exhibit difference in the heart rate (177±13 vs. 155±13 bpm, P=0.08). On 8-hydroxy-2'-deoxyguanosine (8-OHdG), dihydroethidium and dichlorodihydrofluorescein diacetate staining, enhanced oxidative stress was observed in the atrial tissue in the pacing control, but not in the pacing + carvedilol group. CONCLUSIONS: Carvedilol suppressed AF inducibility and oxidative stress in the canine AF model.
AIMS: We evaluated the effect of carvedilol, a beta-blocker with anti-oxidative action, against the atrial fibrillation (AF) inducibility, the development of atrial remodeling and the oxidative stress markers in a canineAF model. METHODS AND RESULTS:AF model was produced by performing 6-week rapid atrial stimulation in 15 dogs. The animals were divided into the following three groups: (I) pacing + carvedilol group (n=5); (II) pacing control group (n=5); and (III) non-pacing group (n=5). AF inducibility was gradually increased along the time course in the pacing control group. In the pacing + carvedilol group, the AF inducibility was suppressed especially in the latter phase of protocol in comparison with the pacing control group. Although carvedilol has beta-blocking effect, pacing control and pacing + carvedilol groups did not exhibit difference in the heart rate (177±13 vs. 155±13 bpm, P=0.08). On 8-hydroxy-2'-deoxyguanosine (8-OHdG), dihydroethidium and dichlorodihydrofluorescein diacetate staining, enhanced oxidative stress was observed in the atrial tissue in the pacing control, but not in the pacing + carvedilol group. CONCLUSIONS:Carvedilol suppressed AF inducibility and oxidative stress in the canineAF model.
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