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作 者:左霞[1] 陈红英[1] 陈德森[2] 李英[1] 王文杰[1] 李贤玉[3]
机构地区:[1]湖北医药学院附属十堰市太和医院骨二科,442000 [2]湖北医药学院机能实验室 [3]湖北医药学院病理生理教研室
出 处:《环球中医药》2015年第4期407-410,共4页Global Traditional Chinese Medicine
基 金:湖北医药学院研究生启动基金(2008QDJ9)
摘 要:目的研究参麦注射液对大鼠脑缺血再灌注损伤的保护作用及机制。方法 SD大鼠40只随机分为对照组、模型组及参麦组,模型组及参麦组均经右侧颈动脉线栓大脑中动脉Willis环,阻断血流30分钟后再灌注30分钟,并反复3次的方法,建立大鼠脑缺血再灌注损伤的模型。采用尾静脉给药,每天1次,连续6天,对照组给予等体积生理盐水。观测缺血再灌注0、30、60分钟及1天、3天、6天共计6个时间点局部脑血流量(regional cerebral blood flow,RCBF)及脑电图(electroencephalogram,EEG)棘波振幅。并计算脑缺血再灌注前及6天后脑梗死范围。结果参麦注射液组在第3天、6天2个时点测得值显示RCBF显著升高、EEG棘波波幅明显降低,显著降低再灌注6天后脑梗死范围,与模型组比较,差异均有统计学意义(P<0.05)。结论参麦注射液对大鼠脑缺血再灌注损伤有保护作用,作用机制可能与其具有抑制大鼠脑缺血再灌注后大脑异常放电,降低血管平滑肌细胞膜Na+-K+-ATP酶活性,松弛脑血管平滑肌改善微循环增加脑血流量有关。Objective To study the protective effect and mechanism of Shenmai Injection on rats with cerebral ischemia reperfusion injury. Methods 40 SD rats were randomly divided into control group,model group and Shenmai Injection group. Model group and Shenmai Injection group were treated by right carotid artery thread embolism of middle cerebral artery Willis ring,blocking blood flow for 30 min and conducting reperfusion for 30 min. This method is repeated 3 times to construct rat models of cerebral ischemia reperfusion injury. Caudal vein administration was conducted,1 times a day for 6 consecutive days.The control group was given normal saline with the same volume as model group and Shenmai Injection group. After ischemia reperfusion for 0,30,60 min and 1d,3d,6d,cerebral blood flow( regional cerebral time blood flow( RCBF) and electroencephalogram( EEG) spike wave amplitude at 6 time spots were observed. Cerebral infarction range before and 6d after cerebral ischemia reperfusion was calculated. Results RCBF increased significantly and EEG spike wave amplitude decreased markedly in the 3rd day and6 th day in the Shenmai Injection group,which significantly reduced the cerebral infarction range after 6d of reperfusion. Compared with the model group,the difference was statistically significant( P〈0. 05). Conclusion Shenmai Injection has protective effect on rats with cerebral ischemia reperfusion injury. The mechanism of action may be associated with the inhibition of abnormal discharge in the rat's brain after cer-ebral ischemia reperfusion,the reduction of enzyme activity of vascular smooth muscle cell membrane Na+-K+- ATP,the relaxation of cerebrovascular smooth muscles,the improvement of microcirculation and the increase of cerebral blood flow.
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