Animal Models of Cerebral Stroke: Pharmacological Protection of Function

We used a photochemical technique which induces thrombotic infarction by intravenous injection of the fluorescein derivative Rose Bengal and focal illumination of the intact skull surface. Following such photochemi-cally induced infarcts in the sensorimotor neocortex of rats, posttreatment with flunarizine, a class IV calcium antagonist, within a critical period of the first 6 h after infarction, results in marked sparing of sensorimotor function (tactile/proprioceptive limb placing reactions), while animals remain normoglycemic and are free of drug-induced behavioral toxicity. This could reflect flunarizine-induced coping of neuronal tissue with ischemia-related ionic shifts. It is argued that photochemical thrombosis and middle cerebral artery occlusion can fruitfully complement each other as experimental stroke models.