Clinical and Experimental Hypertension, 28:387–394, 2006 Copyright © Taylor & Francis Group, LLC ISSN: 1064-1963 print / 1525-6006 online DOI: 10.1080/10641960600549827 387 LCEH 1064-1963 1525-6006 Clinical and Experimental Hypertension, Vol. 28, No. 03, February 2006: pp. 0–0 Clinical and Experimental Hypertension Protection by Apomorphine in Two Independent Models of Acute Inhibition of Oxidative Metabolism in Rodents Apomorphine Protects against Oxidative Metabolism P. Castri et al. PAOLA CASTRI, 1 CARLA BUSCETI, 2 GIUSEPPE BATTAGLIA, 2 FRANCESCA GIRARDI, 1 MICHELE CAVALLARI, 1 FRANCESCO ORZI, 1 AND FRANCESCO FORNAI 3 1 Department of Neurological Sciences, University of Roma, “La Sapienza”, Rome, Italy 2 Neuromed Institute, Pozzilli (Isernia), Italy 3 Department of Human Morphology and Applied Biology, University of Pisa, Pisa, Italy 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. Keywords apomorphine, gerbil, ischemia, mice, MPTP, neuroprotection, oxidative metabolism Introduction There is a growing body of evidence that tissue damage associated with brain ischemia is a process protracted in time rather than a sudden event, and that ischemic cell death is the end-result of a complex cascade of interacting factors. The process itself consists of pathogenetic events traditionally associated with neurodegeneration. The term “acute neurodegeneration” is being used by a number of researchers to describe the slow progression to death that occurs in the penumbral area of the ischemic territory after focal ischemia, or Address correspondence to Prof. Francesco Orzi, Dipertimento di Scienze Neurologiche, Università di Roma “La Sapienza,” Ospedale Sant’ Andrea Via di Grottarossa 1035, 00189 Roma, Italy; E-mail: francesco.orzi@uniroma1.it Clin Exp Hypertens Downloaded from informahealthcare.com by National Institutes of Health Library on 04/18/12 For personal use only.