Abstract
Interaction between adenosine and isoproterenol (ISP) on myocardial inotropic action was studied in open-chest dog hearts. The local myocardial force and the left ventricular (LV) dP/dt were measured as indices of myocardial contractility. Isoproterenol [ISP, 9.47 μM (2μg/ml)] was infused into the left circumflex coronary artery at rates of 0.05ml/min (low dose ISP) or 0.2ml/min (high dose ISP). Two mM adenosine or 0.5mM N6-phenylisopropyl-adenosine (PIA) were infused into the coronary artery at rates of 0.2 (4×10-7 mol/min.), 0.5 (1×10-6 mol/min) and 10ml/min (2×10<-5> mol/min) In the presence of either a low or a high dose of ISP. Adenosine infusion at a rate of 0.2ml/min did not modify myocardial contractility in the presence of the both doses of ISP. The larger doses of adenosine. 0.5ml/min and 10ml/min, decreased myocardial-developed tension and LVmax dP/dt dose-dependently. However, the dose of adenosine which affected myocardial contractility was inphysiologically high in comparison with the concentration in the ischemic myocardium. PIA, a potent agonist of adenosine A1-receptor, attenuated an increase in myocardial contractility in a dose-dependent manner which was caused by intracoronary ISP infusion. This indicates that A1-adenosine receptors exist, but a functional adenosine-catecholamine antagonism does not play a significant role in the canine left ventricle.
