Conclusions
Although the results of this study do not offer compelling support for
the use of diazepam in reducing chloroquine cardiotoxicity, evidence
that it might enhance cardiac contractility when co-administered with
adrenaline is plausibly explained through its PDE-4 inhibitory effects.
However, adrenaline lowered whole blood potassium concentrations,
consistent with agonism of β2-adrenoceptors in skeletal
muscle. As this may exacerbate chloroquine-induced hypokalaemia
(Clemessy et al., 1995) and increase arrhythmogenicity, it is proposed
that treatment of acute chloroquine toxicity should instead include the
administration of a positive inotrope with a greater selectivity for
β1-adrenoceptors, such as dobutamine. Given that
chloroquine poisoning often causes convulsions, which can be
intractable, there may be additional, non-cardiovascular roles for
diazepam treatment.