Abstract
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.
