Objective To study the effects of urinary kallidinogenase (kallikrein) on focal cerebral blood flow (CBF) following cerebral infarction in rats by laser speckle imaging.Methods Permanent middle cerebral artery occlusion (MCAO) was induced in male Sprague-Dawley rats by the intraluminal filament technique.Laser speckle imaging was used to measure CBF in the ischemic cortical area and middle cerebral artery territory.The brain was stained with 2,3,5-triphenyltetrazolium chloride (TTC) to determine the infarct size.Neurological deficit score was measured.Results CBF increased in both hemispheric cortical area and MCA territory on the first and second days following urinary kallikrein administration at high dose but not at low dose.Larger blood vessel diameter and increased blood flow velocity were noticed in the high dose group in some arteries when compared to the low dose group and normal saline control group.At 36 h after cerebral ischemia,the brain infarct size was 10.14% ±3.02% ,25.99% ±3.90% and 27.10% ±3.32% in high, low dose and normal saline control groups,respectively.The infarct size was significantly smaller in the high ( F = 61.14, P<0.01 ) but not low dose group when compared to the normal saline control group.The neurological deficit was milder in the high dose group but not the other two groups at 4 h after cerebral ischemia; however, there were no differences among the groups at 36 h after MCAO.Conclusions Urinary kallidinogenase can reduce cerebral infarction volume and neurological deficit in rats following focal cerebral ischemia.These effects may be attributed to enhanced collateral circulation and improved CBF in the hemispheric cortical area and MCA territory.