Abstract
The hemodynamic effects of a new betablocking agent, acebutolol, dl-1- (2 acetyl-4-butyramidophenoxy) -2-hydroxy-3-isopropylaminopropane hydrochloride were studied in 10 dogs anesthetized with pentobarbital sodium and 33% nitrous oxide in oxygen.
1 mg/kg of acebutolol was given intravenously every 5-7 minutes up to total dose of 5 mg/kg. The administration of increasing doses of acebutolol produced a progressive decrease in heart rate (3 mg/kg, P<0.01), mean arterial pressure (2 mg/kg, P<0.01), left ventricular pressure (3 mg/kg, P<0.01), first derivative of left ventricular pressure (4 mg/kg, P<0.05), peak aortic flow velocity (3 mg/kg, P<0.05), acceleration of aortic flow (4 mg/kg, P<0.05), cardiac output (2 mg/kg, P<0.05), and cardiac work (2 mg/kg, P<0.05), while left ventricular end-diastolic pressure was increased progressively (2 mg/kg, P<0.05). Total peripheral resis tance was not altered significantly. So called Vmax (V' max) as an index of myocardial contractility obtained by extrapolation of the pressure-velocity descending limb to zero load was progressively decreased (3 mg/kg, P<0.05). Based on the fact that heart rate, ventricular wall tension (or ventricular pressure), and myocardial contractility correlates closely with myocardial oxygen consumption, it was postulated from above findings that acebutolol would decrease myocardial oxygen consumption. Acebutolol in a dose which did not significantly depress myocardial contractility (V' max, dp/dt) in normal heart showed an antiarrhythmic effect on epinephrine induced ventricular arrhythmia during halothane anesthesia.
In conclusion acebutolol could be considered as a clinically useful drug to relieve anginal attack and to control cardiac tachyarrhythmia and hypertension. However, it should be emphasized that acebutolol has a possibility to cause heart failure, if it was used in unreasonable high dose.
