Abstract
The purpose of this study was to determine the mean EC50 of adrenaline on heart rate and force of contraction of isolated New Zealand white rabbit hearts and to determine the concentration of atenolol that completely blocks the effect of adrenaline using one of modern physiological acquisition system, PowerLab, AD instrumnets. Twelve Isolated hearts from New Zealand white rabbits were perfused through aorta in a Langendorff mode. Heart rate and contractility were determined for 5 minutes after bolus injection of 5 different concentrations of adrenaline (1.0, 2.5, 5.0, 7.5 and 10 mu g/mL). The changes in heart rate and contractility after each treatment were compared with their baseline values. These data were used to calculate the mean EC50 of adrenaline on heart rate and force of contraction. This EC 50 was then used after perfusion of different concentrations of atenolol (1.0, 2.5, 5.0 and 10 mu g/mL). Data were collected with the help of PowerLab data acquisition and analyzed by Labchart pro7 software. Adrenaline resulted in a stimulatory effect on the heart rate and the amplitude of the heart contraction. The maximum increases in both heart rate and force of contraction were seen at adrenaline dose of 7.5 mu g/mL and the plateau phase was achieved at a dose of 10 mu g/mL. The average EC50 of adrenaline was 3.5 mu g/mL. The positive inotropic effect of adrenaline was antagonized only at atenolol concentrations of 5.0 and 10 mu g/mL and complete inhibition of adrenaline effect on heart rate was achieved at atenolol concentrations of 10 mu g/mL. These data showed that atenolol must be used at a concentration no less than 7.5 mu g/mL to demonstrate if beta adrenergic receptors are involved in the mechanism of action of any newly tested positive inotropic or choronotroic drug.