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尿苷三磷酸对大鼠局灶性缺血再灌注损伤脑组织的保护作用
田谋利1△,孙海静1△,高欣2,宁慧杰1,石学银1*
0
(1.第二军医大学长征医院麻醉科,上海 200003; 2.第二军医大学长征医院影像科,上海 200003)
摘要:
目的采用磁共振成像(MRI)法连续观察尿苷三磷酸(UTP)对大鼠局灶性脑缺血再灌注损伤的作用。方法线栓法制备大鼠中脑缺血再灌注(MCAO)损伤模型,大脑中动脉缺血30 min后以微量输注泵采用大鼠尾静脉持续给予不同剂量的UTP,输注速度为5 ml·kg-1·min-1。再灌注24 h后测量大鼠脑含水量及神经损伤行为学评分(NDS),并采用TTC染色法观察大鼠脑梗死体积。采用MRI连续观察脑缺血再灌注后6、30、54 h大鼠脑梗死情况。结果10、30、90 μg/kg UTP组大鼠NDS评分明显低于生理盐水对照组(P<0.01),大鼠右侧大脑半球含水量明显少于生理盐水对照组(P<0.01)。随着UTP剂量的增加,梗死区域逐渐缩小,10、30、90 μg/kg UTP组梗死体积占整个脑半球体积的百分比均较生理盐水对照组明显减少(P<0.01)。与生理盐水对照组相比,90 μg/kg UTP组再灌注后6、30、54 h梗死区域明显减少,差异有统计学意义(P<0.01)。结论UTP对大鼠局灶性缺血再灌注损伤脑组织具有保护作用,可显著减少脑梗死体积。
关键词:  尿苷三磷酸  再灌注损伤  脑缺血  脑梗死
DOI:10.3724/SP.J.1008.2010.0608
投稿时间:2010-01-04修订日期:2010-05-28
基金项目:
Protective effect of uridine 5’-triphosphate on brain tissue after cerebral ischemia-reperfusion injury in rats
TIAN Mou-li1△, SUN Hai-jing1△, GAO Xin2, NING Hui-jie1, SHI Xue-yin1*
(1. Department of Anesthesiology, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China; 2. Department of Radiology, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China)
Abstract:
ObjectiveTo use MRI method for continuous observation of the protective effect of uridine 5’-triphosphate (UTP) against cerebral ischemia-reperfusion (IR) injury in rats. MethodsThe cerebral ischemia was induced by middle cerebral artery occlusion (MCAO) in rats. UTP solution was delivered through an indwelling tail venous catheter via microinfusion pump 30 min after MCAO at a rate of 5 ml·kg-1·min-1. Neurological deficit score (NDS) and brain water content were determined 24 h after reperfusion. The infarction volume was determined by 2,3,5-triphenyl-tetrazolium chloride (TTC) staining and MRI at 6, 30, and 54 h after reperfusion. ResultsThe NDS scores in 10, 30, and 90 μg/kg UTP groups were significantly lower than that in the saline control group(P<0.01); the water contents in the right cerebral hemisphere of 10, 30, and 90 μg/kg UTP groups were significantly less than that in the normal saline group(P<0.01). The cerebral infarction volume was gradually decreased with the increase of UTP dose, and the proportions of infarction volumes in 10, 30, and 90 μg/kg UTP groups were significantly decreased compared with the saline control group(P<0.01). The infarction volumes at 6, 30, and 54 h after reperfusion in 90 μg/kg UTP group were significantly lower than those in the saline control group(P<0.01). ConclusionUTP has a protective effect on focal cerebral ischemia-reperfusion injury in rats; it can greatly reduce the volume of cerebral infarction.
Key words:  uridine triphosphate  reperfusion injury  brain ischemia  brain infarction