Use of laser speckle imaging to study effects of urinary kallidinogenase on cerebral blood flow following cerebral infarction in rats
10.3760/cma.j.issn.1006-7876.2010.10.016
- VernacularTitle:利用激光散斑成像技术观察尤瑞克林对脑梗死大鼠脑血流的影响
- Author:
Changsheng LI
;
Zhe MIN
;
Yanqiang ZHAN
;
Jie XU
;
Lianchen XIAO
;
Suming ZHANG
- Publication Type:Journal Article
- Keywords:
Infarction,middle cerebral artery;
Kallikreins;
Regional blood flow;
Lasers;
Diagnostic imaging;
Disease models,animal
- From:
Chinese Journal of Neurology
2010;43(10):732-736
- CountryChina
- Language:Chinese
-
Abstract:
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.
