Objective: To evaluate the effect of amrinone as a treatment for the h
emodynamic effects of verapamil overdose in a canine model. Methods: T
his nonblind interventional study was performed in an established cani
ne model of verapamil toxicity, without concurrent control animals, Pe
ntobarbital-anesthetized and instrumented dogs (n = 8) were maintained
and observed for 60 minutes or until death, The animals were overdose
d with verapamil, 15 mg/kg IV, over 30 minutes. Hemodynamic parameters
, including cardiac index (CI), heart rate (HR), and mean arterial pre
ssure (MAP), were monitored. Completion of the verapamil infusion repr
esented the defined point of toxicity; at that point, all the animals
received an amrinone bolus of 2 mg/kg IV over 2 minutes followed by an
amrinone drip at 10 mu g/kg/min. The hemodynamic values at the define
d point of toxicity were compared with those obtained postinitiation o
f the amrinone infusion. Results: Two animals died before the 60-minut
e observation period elapsed, Baseline CI was 5.6 L/min/m(2). Followin
g verapamil-induced toxicity, mean CI was 2.2 L/min/m(2). After admini
stration of amrinone, a significant (p < 0.05) increase in CI was obse
rved at 30 minutes (CI = 3.6 L/min/m(3)), 45 minutes (CI = 4.2 L/min/m
(2)), and 60 minutes (CI = 4.2 L/min/m(2)). There was no statistically
significant difference noted for MAP or HR compared with ''point of t
oxicity'' values. Conclusion: Amrinone appears to reverse the depresse
d cardiac index associated with verapamil overdose in a canine model w
hile having no significant effect on the hypotension or bradycardia.