Protection by apomorphine in two independent models of acute inhibition of oxidative metabolism in rodents.

Apomorphine was administered by continuous infusion in the mouse following acute inhibition of oxidative metabolism induced by systemic administration of MPTP, and in the gerbil following transient occlusion of the carotid arteries. The dosage employed was comparable to the one used in the treatment of severe on-off fluctuations in Parkinson's disease. The results show that apomorphine significantly diminishes the striatal lesion caused by MPTP and the size of the infarct associated with the transient global ischemia. These data suggest that apomorphine is neuroprotective, probably by means of an antioxidant effect, at doses that are clinically used. The finding may be relevant to brain ischemia as well to chronic neurodegeneration.