Thesis (M.Sc.)--Chulalongkorn University, 2004

The objective of the present study was to investigate the effects of vasodilators (beta[subscript 2]-adrenergic agonist and alpha[subscript 1]-adrenergic antagonist) on cardiac contractility and arrhythmogenesis in ischemic induced - rat hearts. Sixty male spraque-dawley rat hearts were randomized into 4 groups: the first group was perfused with Krebs- Henseleit bicarbonate (KHB) buffer and used as control group; the second group was perfused with KHB buffer and 10 micrometre atenolol (ATEN); the third group was perfused with KHB buffer 10 micrometre atenolol and 0.01 micrometre salbutamol (ATEN/SALBU); the fourth group was perfused with KHB buffer, 10 micrometre atenolol and 5 micrometre prazosin (ATEN/PRAZ). Rat hearts were isolated and mounted in Langendorff apparatus. Left ventricular developed pressure, dP/dt[subscript max] and dP/dt[subscript min], Vmax, ECG, coronary flow, and RR-variability were recorded and determined. After drug perfusion for 10 minutes, the left anterior descending artery was occluded for 8 minutes and then reperfused to induce cardiac arrhythmias. Coronary flow and heart rates increased after ATEN/SALBU perfusion and decreased after ATEN/PRAZ. Ischemia deteriorated cardiac contractility and coronary flow in all treated groups. Recovery of contractile function and coronary flow were observed after reperfusion. Ischemic-reperfusion induced sustained ventricular fibrillation in all groups except ATEN/PRAZ treated group. Increases in cardiac myocyte apoptosis induced by adrenergic drugs were not observed in this study. In conclusion, the combination of beta[subscript 1]-antagonist and alpha[subscript 1]-antagonist has antiarrhythmic action in ischemic-induced rat heart. However, beta[subscript 2]-agonist showed vasodilatory effect and increases in cardiac contractility.