The effects of isradipine in a rat model of embolic stroke [permanent occlusion 
of the left middle cerebral artery (MCA)] are reviewed. Isradipine, when present 
or given up to 4 hours after the onset of stroke, reduces the infarct size, 
determined by magnetic resonance imaging (MRI) 24 hours, and by histology 5 
days, after MCA occlusion. These cytoprotective effects seem to be permanent and 
are paralleled by an improvement in the neurological deficit. Isradipine has 
proved to be the most potent and effective calcium antagonist for reducing the 
infarct size compared with other representatives of this class of drugs such as 
nimodipine, nicardipine and flunarizine. Isradipine is cytoprotective after a 
stroke when used as an antihypertensive: at doses which normalise high blood 
pressure in spontaneously hypertensive rats, isradipine reduces by more than 60% 
the infarct size caused by a subsequent stroke. Since the lowering of blood 
pressure, e.g. by a calcium antagonist that does not cross the blood-brain 
barrier, is ineffective in reducing the infarct size, normalisation of blood 
pressure alone cannot account for the reductions in infarct size observed with 
isradipine. The antihypertensive drug isradipine seems rather to offer the 
additional benefit of attenuating the consequences of an eventual stroke. If 
clinically confirmed, this will be of considerable therapeutic importance. 
Evidence is presented that isradipine has at least 2 mechanisms within the brain 
that might be responsible for cytoprotection in stroke.(ABSTRACT TRUNCATED AT 
250 WORDS)