参附注射液对大鼠短暂性局灶性脑缺血损伤的保护作用

目的探讨参附注射液对脑缺血性损伤的保护作用及量效关系。方法40只雄性SD大鼠，随机分为4组，对照组（n=10），即缺血再灌注组，在缺血前30分钟经腹腔注射生理盐水20ml/kg；各保护组（Cen5,Cen10,Cen20,各组n=10）在缺血前30分钟经腹腔注射参附注射液(剂量分别为5、10、20ml/kg)及生理盐水(剂量分别为15、10、0ml/kg)。采用右侧颈内动脉丝线栓塞致大脑中动脉阻闭120分钟，术后观察1、3、6、12、16和24小时神经行为学变化并评分，24小时时处死动物，取大脑行TTC染色以测量脑梗死容积。结果24小时神经功能评分，各保护组为Cen5〔(0.6±0.5)分,P<0.05〕,Cen10〔(0.8±0.9）分,P<0.05〕,Cen20〔(0.7±0.4)分,P<0.05〕，均明显低于对照组〔(1.8±1.0)分〕；24小时梗死容积各保护组为Cen5〔(58.7±21.4)mm

Protective effect of Shenfu injection(

Objective:To investigate the protective effec ts of Shenfu injection(参附注射液) on transient focal cerebral ischemic injury i n rat and doseresponse relation.Methods:Forty male SD rats (body weight 350400 g) were randomly divided into 4 groups.In control group (ischemiarep erfusion group,n=10),30 minutes before ischemia the normal saline 20 ml/kg was injected int o peritoneal cavity otherwise in all protective groups,including Cen 5(n=10),Cen10(n=10),and Cen20(n=10) group,30 minutes before ischemia the Shenfu injection (dosage 5,10 and 20 ml/kg respectiv ely) and normal saline (dosage 15,10 and 0 ml/kg respectively) were injected int o peritoneal cavity.By means of ligating the right carotid artery to obstruct th e cerebral middle artery for 120 minutes,at 1,3,6,12,16 and 24 hours after obstr uction the changes in neurological behavior were observed and scored.At 24 hours the rats were killed and the volume of cerebral infarction was measured using T TC stain.Results:The neurologic deficit scores (NDS) in group Cen5,group Cen10 and group Cen20 at 24 hours after reperfusion were (0.6±0. 5 )scores,(0.8±0.9)scores and (0.7±0.4)scores respectively and significantly lower than that in control group (1.8±1.0)scores(all P<0.05). The infarct volume in control group 〔(17 9.5±45.2）mm3〕 was significantly higher than those in group Cen5 〔(58.7±21.4）mm3,P<0.05〕，Cen10 〔(61.5±28.7）mm 3,P<0.05〕 and Cen20 〔（31.2±20.6）mm3,P<0.01〕 .Among all the Shenfupretreated groups both NDS and infarct volume h ad not differences.Conclusions:The Shenfu injection possesses dosageindependent protective effects on transient focal cerebral ischemic injury.