CAJ | 학술논문

目的利用激光散斑成像技术研究尤瑞克林对大鼠脑梗死后局部脑血流的影响.方法成年雄性SD大鼠24只,线栓法制备大鼠永久性大脑中动脉梗死模型.激光散斑成像系统观测缺血半球皮质及大脑中动脉供血区血流,2,3,5-三苯基氯化四氮唑(TTC)染色法测定脑梗死体积,并进行神经功能评分.结果皮质及大脑中动脉供血区血流在大剂量组第1天及第2天给药后均有明显改善,部分大脑皮质血管增粗,血流速度加快,小剂量组及生理盐水组无明显变化,脑缺血48 h后,大、小剂量尤瑞克林组及生理盐水组的梗死体积分别为10.14%±3.02%,25.99%±3.90%,27.10%±3.32%,大剂量组与生理盐水组比较差异有统计学意义(F=61.14,P<0.01),小剂量组与生理盐水组比较差异无统计学意义.缺血后4 h,大剂量组神经功能损伤明显改善,小剂量组及生理盐水组无明显改变,36 h各组间的神经功能评分差异无统计学意义.结论尤瑞克林可以减少大鼠局灶性脑缺血后梗死体积,延缓神经功能损伤,其作用可能与促进侧支循环的开放,增加大脑皮质和缺血区血流有关.
목적 이용격광산반성상기술연구우서극림대대서뇌경사후국부뇌혈류적영향.방법 성년웅성SD대서24지,선전법제비대서영구성대뇌중동맥경사모형.격광산반성상계통관측결혈반구피질급대뇌중동맥공혈구혈류,2,3,5-삼분기록화사담서(TTC)염색법측정뇌경사체적,병진행신경공능평분.결과 피질급대뇌중동맥공혈구혈류재대제량조제1천급제2천급약후균유명현개선,부분대뇌피질혈관증조,혈류속도가쾌,소제량조급생리염수조무명현변화,뇌결혈48 h후,대、소제량우서극림조급생리염수조적경사체적분별위10.14%±3.02%,25.99%±3.90%,27.10%±3.32%,대제량조여생리염수조비교차이유통계학의의(F=61.14,P<0.01),소제량조여생리염수조비교차이무통계학의의.결혈후4 h,대제량조신경공능손상명현개선,소제량조급생리염수조무명현개변,36 h각조간적신경공능평분차이무통계학의의.결론 우서극림가이감소대서국조성뇌결혈후경사체적,연완신경공능손상,기작용가능여촉진측지순배적개방,증가대뇌피질화결혈구혈류유관.
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.