S. Sato et al., COMBINED USE OF GLUCAGON AND MILRINONE MAY NOT BE PREFERABLE FOR SEVERE PROPRANOLOL POISONING IN THE CANINE MODEL, Journal of toxicology. Clinical toxicology, 33(4), 1995, pp. 337-342
In a previous study of propranolol poisoning, glucagon and milrinone s
ignificantly increased cardiac output, but the improvement caused by g
lucagon was almost entirely due to the chronotropic effect. This study
investigates the combined effect of glucagon, in a dose not inducing
tachycardia, and milrinone on beta-blocker poisoning. Following the ad
ministration of 10 mg/kg propranolol IV over ten minutes, dogs (N = 20
) were divided into four treatment groups, group S (saline), group G (
glucagon 2.5 mu g/kg), group M (milrinone 100 mu g/kg), and group G M (glucagon 2.5 mu g/kg plus milrinone 100 mu g/kg). Hemodynamic param
eters were observed over the next thirty minutes. Heart rate, cardiac
output, and mean arterial pressure were decreased in all groups after
the administration of propranolol. Heart rate, mean arterial pressure,
cardiac output, and stroke volume recovered to the baseline values in
group G + M. However, heart rate in group G + M showed a significant
increase versus the other three groups. In a canine model of severe pr
opranolol poisoning, the combined effect of glucagon 2.5 mu g/kg and m
ilrinone 100 mu g/kg brought about a significant hemodynamic improveme
nt, bur it was accompanied by an excessive increase of heart rate, Com
bined therapy of milrinone and glucagon may not be preferable therapy
in beta-blocker poisoning in the canine model.