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Revista Espanola de Cardiologia 2010-Apr

[Adenosine induces ventricular arrythmias in hearts with chronic chagas cardiomyopathy].

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Edilmar Alvarado-Tapias
Marianna Rivas-Coppola
Alfonso Alvarado
María Bello
Mario Briceño
Claudina Rodríguez-Bonfante
Rafael Bonfante-Cabarcas

Ključne riječi

Sažetak

Adenosine released during ischemia and hypoxia can induce ventricular arrhythmias. This phenomenon is also observed in Chagas disease. This study involved pharmacologic analysis of the arrhythmogenic properties of adenosine in healthy Sprague-Dawley rats (n=14) and in rats with chronic Chagas cardiomyopathy (n=14). Electrocardiographic and pharmacologic studies were performed on isolated hearts prepared using the Langendorff method. Adenosine increased ventricular arrhythmias in both groups of animals in a dose-dependent manner: 50% of chagasic rats developed ventricular fibrillation compared with 7.14% of healthy rats (P< .05). Fibrillation was prevented by A1 (i.e., DPCPX) and A2a (i.e., 8-CSC) receptor antagonists. Arrhythmia was associated with a prolonged QT interval, early depolarization, and the R-on-T and torsade de pointes phenomena. In conclusion, adenosine is a proarrythmic drug that is able to induce ventricular fibrillation in chagasic rat hearts.

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