Increased sympathetic tone is a consequence of cerebral ischemia. Although the role of catecholamines in ischemic damage is still unclear, in some experimental ischemia models alpha2-adrenergic agonism has proved to be neuroprotective. In the present work we have compared the effects of transient and permanent middle cerebral artery occlusion (MCAO) on the infarct volume, and, also, examined whether a selective alpha2-adrenergic receptor agonist, dexmedetomidine (9 microg/kg or 15 microg/kg i.v.), is able to reduce ischemic damage after transient or permanent MCAO in rats. Permanent MCAO led to a significantly larger infarct volume than transient occlusion (p < 0.05). The rats receiving the higher dose of dexmedetomidine were detectected to have smaller (statistically non-significant) infarct volume in the cortex (30.9%) and in the striatum (20.3%) after transient occlusion. Additionally, dexmedetomidine caused significant variations in the physiological parameters.