摘要
结扎犬脑基底动脉后６ｈ，发现脑干听觉诱发电位ＢＡＥＰ，各波的峰潜伏期（ＰＬ）及峰间期（ＩＰＬ）明显延长（Ｐ＜０．０１）；脑干神经元形态结构发生缺血性改变（光镜及电镜），脑干组织ＰＬＡ２活性升高５．８倍（Ｐ＜０．０１），超氧化物歧化酶（ＳＯＤ）活性降低５８．８％（Ｐ＜０．０１）。海风藤３００ｍｇ·ｋｇ－１、氟桂嗪１ｍｐ·ｋｇ－１、绞股蓝皂甙１５０ｍｇ·ｋｇ－１，分别于结扎脑基底动脉前３ｈ经十二指肠造瘘管给药，皆能缩短ＰＬ及ⅠＰＬ的延长（Ｐ＜０．０１），明显减轻神经元形态结构的缺血性改变，三者作用相当。与缺血组相比较，三药分别使ＰＬＡ２活性降低８０．２％。７４．２％和７２．４％（Ｐ＜０．０１），使ＳＯＤ活性升高２．１、１．９５和１．８４倍（Ｐ＜０．０１）。上述结果提示三药抗脑缺血损伤的作用与其降低ＰＬＡ２活性和增强ＳＯＤ活性有关。
A brainstem ischemia model was established in dogs. It was shown that six hours (h) after brainstem ischemia, the ischemic neuronal damage (histopathologically evaluated by light and electronic microscope) was observed, the peak latencies (PL) and inter-peak latencies (IPL) of the BAEP increased significantly, the PLA2 activity of brainstem hemogenate increased 5.8 times than that of control group (P<0.01), SOD activity of brainstem hemogenate reduced by 58.8 percent of the control. Piper willchii (0.3g.kg-1), gypenoside (150mg.kg-1) and flunanize (1mg.kg-1) intraduodinal administered at 3h before ischemia, attenuated the ischemic neuronal damage, ameliorated the abnormal changes of BAEP(P<0.01). The three drugs had similar protective effects. All of the three drugs reduced the PLA2 activity (by 80.2, 74.2 and 72.4 percent of that in control groups, respectively)(P<0.01)and increased SOD activity (2.1, 1.95 and 1.84 times than that of control groups, respectively)(P<0.01). the result suggests that the protective mechanism of the three drugs may be related to the inhibition of PLA2 cativity and the increase in activation of SOD.
出处
《中国神经精神疾病杂志》
CAS
CSCD
北大核心
1996年第2期88-90,共3页
Chinese Journal of Nervous and Mental Diseases
关键词
脑缺血
海风藤
氟桂嗪
绞股蓝皂甙
中医药疗法
Cerebral ischemia
Neuroprotection
Piper Willchii
Flunanize
Gypenoside
