摘要
目的：探讨三七总皂甙（ＰＮＳ）对脑缺血后的脑保护作用机制。方法：家兔１８只，随机分３组（每组６只）。戊巴比妥钠麻醉，机械通气，阻断双侧颈总动脉和椎动脉，合并放血降压，使脑完全性缺血２０分钟后，松开阻断的动脉，快速回输放出的血液，制成兔完全性缺血再灌注脑模型。再灌注５分钟时，ＰＮＳ组静注ＰＮＳ１５０ｍｇ／ｋｇ；假手术组与缺血对照组均静注等量平衡液。结果：再灌注后１，２和３小时，缺血对照组动脉血超氧化物歧化酶（ＳＯＤ）活性和丙二醛（ＭＤＡ）浓度分别显著低于和高于ＰＮＳ组（Ｐ＜０．０５和＜０．０１）；再灌注３小时后的大脑皮层ＭＤＡ和游离脂肪酸含量，ＰＮＳ组〔分别为（２．５７±０．５０）μｍｏｌ／ｇ和（１９．７８±０．７８）ｍｍｏｌ／ｇ〕均显著低于缺血对照组〔分别为（４．４９±０．３０）μｍｏｌ／ｇ和（２７．３６±０．８４）ｍｍｏｌ／ｇ〕，Ｐ均＜０．０１。
Objective:To explore possible mechanism underlying protective effect of panax notoginseng (PNS) on brain damage after acute cerebral ischemia.Methods:After pentobarbital anesthesia with mechanical ventilation,complete cerebral ischemia in rabbits was induced by occluding both bilateral carotid and vertebral arteries,associated with hemorrhagic hypotension.At the end of 20 minutes ischemia,the occlusion of four vessels was removed and shed blood was rapidly reinfused,followed by 3 hours reperfusion.5 minutes after reperfusion,PNS group ( n =6) received PNS (150 mg/kg),both the shamoperated and ischemia control groups were intravenously infused the same volume balance liquid.Results:At 1,2 and 3 hours after reperfusion,both arterial superoxide dismutase (SOD) activity and malondialdehyde (MDA) concentration were significantly higher and lower in PNS group respectively than the corresponding values in ischemia control group ( P <0 05 or P <0 01).At 3 hours of reperfusion,both MDA and free fatty acid(FFA) contents in cerebral cortex were significantly lower in PNS group,compared with the those of ischemia controls MDA:(2 57±0 50)μmol/g vs.(4 49±0 30)μmol/g, P <0 01;FFA:(19 78±0 78)mmol/g vs.(27 36±0 84)mmol/g, P <0 01 . Conclusions: It is suggested that PNS has the protective effect on acute cerebral damage through scavenging oxygen free radicals and ameliorating of postischemicreperfusion injury.
出处
《中国危重病急救医学》
CAS
CSCD
1999年第3期145-147,共3页
Chinese Critical Care Medicine
关键词
三七皂甙
超氧化物歧化酶
丙二醛
脑缺血
panax notoginseng\ \ superoxide dismutase\ \ cerebral ischemiareperfusion\ \ malondialdehyde
