Evidence against the adenosine-catecholamine antagonism in the canine heart in situ.

Adenosine has been reported to attenuate the positive inotropic effects of catecholamines in isolated heart preparations of rodents. These results were not confirmed in anesthetized dogs during intracoronary infusion of isoprenaline. However, these experiments did not establish the effects of adenosine on the inotropic effects of endogenously released catecholamines. Therefore cardiac sympathetic nerve stimulation was performed in 5 anesthetized, vagotomized dogs. The left circumflex coronary artery was perfused at a constant pressure of 130 +/- 4 mmHg. The contractile function of the circumflex-perfused myocardium was analyzed by sonomicrometry. Cardiac sympathetic nerve stimulation at 1, 2, 5, 10 and 20 Hz increased systolic segment shortening in a frequency-dependent manner from 10.9 +/- 2.6 at control to 15.3 +/- 3.4% at 20 Hz. During intracoronary infusion of adenosine (50 micrograms/kg/min) cardiac sympathetic nerve stimulation still increased systolic segment shortening from 9.9 +/- 3.5 at control to 16.3 +/- 4.5% at 20 Hz. The lack of an adenosine-catecholamine antagonism in the present experiments was not due to the sequence of procedures, nor to the marked flow increase induced by adenosine, since systolic segment shortening at rest was reduced during adenosine infusion, and since during intracoronary infusion of papaverine and sodium nitroprusside similar results were obtained. The observation of an adenosine-catecholamine antagonism in rodents should be restricted to this species at present.