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 photochemically 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.