大鼠脑缺血再灌组织中补体沉积及降纤酶干预的实验观察

被引:9
作者
罗晓光
李绍英
曲恒春
刘亢丁
苏志强
机构
[1] 中国医科大学附属第一临床医院神经内科!沈阳
[2] 不详
[3] 中国医科大学附属第一临床医院胸科实验室
[4] 白求恩医科大学附属第一临床医院神经内科
[5] 哈滨医科大学附一院神经内科
关键词
脑缺血; 缺血再灌损伤; 补体; 蛇毒;
D O I
暂无
中图分类号
R743.32 [脑血栓形成];
学科分类号
摘要
目的本实验旨在观察脑缺血再灌损伤中是否有补体参与,其参与是否与组织坏死有关,蛇毒制剂降纤酶对其有无干预作用。方法制成大鼠大脑中动脉缺血2h再灌22h动物模型,运用免疫组化方法检测再灌组织中的补体沉积,并给予降纤酶处理,观察其干预效果。结果补体C3在缺血再灌组织中大量沉积,为强阳性;降纤酶干预后补体沉积减少,为弱阳性;正常组及假手术组脑组织中无补体沉积。经X2检验证实补体沉积与组织坏死关系密切(P<0.01)。给药组白细胞浸润较未给药组明显减少(P<0.05),组织损伤程度也相对较轻。结论脑缺血再灌组织中有大量补体参与,补体的参与同组织坏死有密切关系。蛇毒制剂降纤酶可减少缺血再灌组织中补体的沉积,从而削减白细胞浸润,减轻脑组织损伤程度。
引用
收藏
页码:203 / 208
页数:6
相关论文
共 10 条
[1]  
Mechanism of complement activation after coronary arteryocclusion evidence that myocardial ischemia in dogs causes release of constituents of myocardial subcellu-lar origin that complex with human Clq in vivo. Rossen RD,Michael LH,Kagiyama A,et al. Circulation Research . 1988
[2]  
Complement localization and mediation of ischemic in-jury in baboon myocardium. Pinckard RN,Orourbe RA,Crawford MH,et al. The Journal of Clinical Investigation . 1980
[3]  
Chemotactic response to human C3a and C5a anaphyla-toxins evaluation of C3a and C5a leukotaxis in vitro and under simulated in vivo conditions. Fernandez HN,Henson PM,Otanl,A,et al. J Immunol . 1978
[4]  
The control of homologous lysis. Lachmann PJ. Immunology Today . 1991
[5]  
Reduction by cobra venom factor of myocardial necrosisafter coronary artery occlusion. Maroko PR,Carpenter CB,Chiariello M,et al. The Journal of Clinical Investigation . 1978
[6]  
Cholesterol and atheroma lipids activate comple-ment and stimulate granulocytes:A possible mechanism for amplification of ischemic injury inatherosclerotic states. Hammerschmidt DE,Greenberg CS,Yamada O,et al. Journal of Laboratory and Clinical Medicine . 1981
[7]  
Complement and neutrophil activation in the pathogenesisof ischemic myocardial injury. Crawford MH,Grover FL,Kolb WP,et al. Circulation . 1988
[8]  
Regulation of complement membrane attack complex formation in my-ocardial infarction. Vakeva A,Laurila P,Meri S. American Journal of Pathology . 1993
[9]  
Polymorphonuclear leukocytes and monocytes/macrophages in thepathogenesis of cerebral ischemia and stroke. Kochanek PM,Hallenbeck JM. Stroke . 1992
[10]  
Reversible middle cerebral artery occlusion without craniectomy in rats. Longa EZ,Weinstein PR,Carlson S,et al. Stroke . 1989