尤瑞克林联合奥扎格雷钠对大鼠脑梗死急性期脑血量的影响

Effects of Urinary Kallidinogenase Combined with Sodium Ozagrelon Cerebral Blood Flow at Acute Stage of Rats with Cerebral Embolism

目的:观察尤瑞克林联合奥扎格雷钠对大鼠脑梗死急性期脑血量的影响。方法:将健康SD大鼠32只随机平均分为尤瑞克林组、奥扎格雷钠组、联合用药组和生理盐水组,进行脑梗死成模,在成模后30min后尾静脉注射给药,尤瑞克林组给予8.75×10-3 PANU/kg尤瑞克林、奥扎格雷钠组给予80mg奥扎格雷钠、联合用药组给予尤瑞克林8.75×10-3 PANU/kg和奥扎格雷钠80mg,生理盐水组给予生理盐水给药;测定用药后10、30、60min局部脑血流(rCBF)、缺血后24h时脑梗塞面积,脑组织切片HE染色结果。结果:尤瑞克林组和奥扎格雷钠组、联合用药组在用药后10、30、60min时,模型脑缺血半暗带rCBF较基线值提高百分比高于生理盐水组(P<0.05),联合用药组高于尤瑞克林组和奥扎格雷钠组(P<0.05);尤瑞克林组、奥扎格雷钠组、联合用药组模型脑梗死面积明显小于生理盐水组(P<0.05),联合用药组脑梗死面积小于尤瑞克林组、奥扎格雷钠组奥扎格雷钠组联合用药组;HE染色可见生理盐水组神经细胞大量变性、坏死、固缩,细胞轮廓不清晰,联合用药组缺血区有部分神经细胞衰亡,较尤瑞克林组和奥扎格雷钠组单独给药相比有明显的改善。结论:尤瑞克林和奥扎格雷钠对于大鼠脑梗死急性期脑血量能明显改善,联合用药时效果更为明显。

Objective:To study effects of urinary kallidinogenase combined with sodium ozagrel on cerebral blood flow at acute stage of rats with cerebral embolism.Methods:With healthy SD rats hypertension models had been established and cerebral embolism models caused by blockages in the circulatory system also had been established.The rat models had been made by the suture method and then divided into the group with urinary kallidinogenase,the group with sodium ozagrel,the group with both urinary kallidinogenase and sodium ozagrel and the group with saline(placebo).The changes in blood pressure had been observed in the course of drug delivery and the regional cerebral blood flow had been detected and cerebral embolism area had been measured after drug delivery,slices of brain tissue and HE staining detected.Conclusions:1The urinary kallidinogenase combined with sodium ozagrel has an obvious effect on blood pressure in treatment of patients with cerebral infarction complicated with hypertension.Combined medication can significantly improve neurological function of large cerebral infarction,and is particularly effective to cerebral thrombosis caused by vertebral artery.2Effects of the urinary kallidinogenase combined with sodium ozagrel on the cerebral infarction area caused by vertebral artery are obvious,can reduce neuronal cell death after the formation of cerebral infarction and improve ischemia-induced inflammatory response.