Episodes of sustained paroxysmal supraventricular tachycardias can be terminated by antiarrhythmic drugs given intravenously. The cardiodepressive effects of these drugs are an important limitation of this therapeutic procedure. The dose-dependent circulatory and myocardial effects of the nucleoside adenosine (0.5, 2.0, 5.0 mg/kg/minute) and the class I antiarrhythmic drug ajmaline (1.0, 2.0, 4.0 mg/kg) were investigated in 73 open-chest rats. Hemodynamic measurements in the intact circulation and isovolumic registrations (peak isovolumic left ventricular systolic pressure and peak isovolumic dP/dtmax) were compared with saline controls. Adenosine has a short-lasting, negative, chronotropic effect that causes a dose-dependent reduction of cardiac output (-34%, -54%, -65% vs control). The peak isovolumic left ventricular systolic pressure (LVSP) is not changed significantly by adenosine (-6%, -4%, +5% vs control). The negative chronotropic effect of ajmaline with consecutive reduction of cardiac output is less pronounced (cardiac output: -18%, -20%, -38% vs control). The highest dose of ajmaline causes a significant reduction of peak isovolumic LVSP (-2%, -1%, -7% vs control). Adenosine has an impressive negative chronotropic effect with a consequent marked decrease of cardiac output. The reduction of cardiac output by adenosine is more pronounced compared with ajmaline. Nevertheless, adenosine has-in contrast to ajmaline-no cardiodepressive effects in vivo.