Why the study?
Does bunazosin infusion reduce myocardial contractility in the beta-blocked canine heart?
Does bunazosin infusion reduce myocardial contractility in the beta-blocked canine heart?
Alpha1-adrenoceptor blockade with bunazosin significantly reduces myocardial contractility in the beta-blocked canine heart.
Alpha1-blockade may reduce contractility despite beta-blockade; leaves open relevance to human HF therapy.
We used the left ventricular (LV) end-systolic force-diameter (Fes-Des) relation to evaluate the effect of an alpha1-adrenoceptor antagonist (bunazosin hydrochloride) on the contractility of the beta-blocked left ventricle. Nine adult mongrel dogs were instrumented with ultrasonic crystals to measure LV diameter and a micromanometer to measure LV pressure. Beta-adrenergic and vagal blockade was induced with intravenous propranolol (2 mg/kg) and atropine (0.2 mg/kg), respectively, and preload was decreased by inferior vena caval occlusion. The slope (Ec) and extrapolated diameter intercept (Do) of the LV Fes-Des relation were derived from end-systolic data obtained in the control state (after beta-blockade) and after bunazosin infusion (1 mg/kg). Ec was used as a new index of LV contractility. After bunazosin infusion, the heart rate and Ec were decreased by 7 and 22%, respectively, in comparison with the control state, whereas Do did not change. These results indicate that alpha1-adrenoceptor blockade significantly reduces myocardial contractility in the beta-blocked canine heart, perhaps by decreasing the intracellular calcium concentration and/or myosin ATPase activity.
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Takeda et al. (1992) studied this question. Bunazosin hydrochloride vs. Control state (after beta-blockade) was evaluated on Slope (Ec) of the left ventricular end-systolic force-diameter relation.
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