The Thai Journal of Veterinary Medicine


Sixty male Spraque-Dawley rats were used in this study. The hearts were isolated and placed on a constant-pressure Langendorff apparatus, and perfused with only Krebs-Henseleit buffer (control), atenolol, atenolol plus prazosin, and atenolol plus salbutamol. After that the left anterior descending artery was occluded for 8 minutes and reperfused for 30 minutes to induce cardiac arrhythmias. The left ventricular pressure and coronary flow rate were monitored, and ECGs were recorded to evaluate cardiac arrhythmias. The administration of atenolol (β1-adrenergic antagonist) combined with prazosin (α1-adrenergic antagonist) prolonged RR intervals whereas that of atenolol combined with salbutamol (β2-adrenergic antagonist) did not prolong RR intervals during the ischemic period. Moreover, reperfusion induced sustained ventricular fibrillation in all groups except the atenolol plus prazosin treated group. The decline of coronary flow rate after reperfusion in atenolol and atenolol plus salbutamol treated groups were lower than the atenolol plus prazosin group. Our results support the theory that α1-adrenergic receptors play an important role on reperfusion arrhythmia whereas coronary vasodilation is mediated through β2-adrenergic receptors. Furthermore, the combination of β1-adrenergic antagonist and α1-adrenergic antagonist could have a more beneficial effect for anti-arrhythmia in cardiac ischemia.



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