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.