期刊文献+

脑卒中后遗症“气虚血瘀”模型大鼠运动功能与神经元突触的变化 被引量:2

Changes of motor function and neurons synapse of the stroke sequela models of rats with deficiency of qi and blood stasis
下载PDF
导出
摘要 目的:观察大鼠运动功能与脑组织神经元突触结构的变化,探讨脑卒中后遗症“气虚血瘀”大鼠病证模型的病理机制。方法:试验于2004-06在南方医科大学中医系实验室完成。选用30只Wistar大鼠,随机分成脑卒中后遗症组,脑卒中急性期组及对照组。复制脑卒中后遗症“气虚血瘀”大鼠模型,运用走横木,电子显微镜和图像分析仪方法。结果:脑卒中后遗症组大鼠与对照组、脑卒中急性期组大鼠比较,除有左上肢内收无力,攀爬鼠笼时向一侧倾倒,下肢外展、内收困难,走路、跳跃时呈跛行状态;有面瘫症状,左眼小,右眼大;提起鼠尾时大鼠不能正常卷起身体,只能不停抖动身体;左侧睾丸萎缩等脑卒中后遗症症状外,还有毛发暗淡无光泽、卷曲,精神委靡,表情惊恐,消瘦,肢体无力,大便稀溏,摄食,饮水减少,手术伤口愈合迟缓等中医“气虚血瘀”征候。脑卒中后遗症组大鼠运动功能评分为(6.00±0.18)分,显著高于脑卒中急性期组犤(4.33±1.67)分,P<0.01犦,脑卒中后遗症组大鼠同对照组、脑卒中急性期组大鼠的突触形态结构比较,缺血区(大鼠脑内坏死边缘区)突触数目(8.33±0.91)明显增多(P<0.05),突触间隙犤(10.13±0.56)nm犦明显变窄(P<0.05),突触活性区长度犤(127.12±10.38)nm犦明显变长(P<0.05),突触后膜致密物质厚度犤(76.78±3.45) AIM:To observe the change of motor function and structure of neurons synapse in brain tissue of the stroke sequela models of rats with deficiency of qi and blood stasis, and probe into the pathological mechanism of the stroke sequela models of rats manifested as syndrome of qi deficiency and blood stasis. METHODS:Totally 30 Wistar mice were randomly divided into stroke sequela group,acute stroke group and control group.The experiment was finished in the Department of Traditional Chinese Medicine,Southern Medical University in June 2004.The stroke sequela models of rats with deficiency of qi and blood stasis were made.Balance beam,electron microscope and image analyzing apparatus were used. RESULTS:As compared with control group and acute stroke group,mice in stroke sequela group had the symptoms that hair was dim and curly,depresse,emotional panic,thinness, asthenic limbs, watery stool,ingestion and drinking decrease,operative scar healing retardation,etc., which were coincident to the sign of qi deficiency and blood stasis which belong to the traditional Chinese medicine besides symptoms of the stroke sequela which adduction of left upper limp was disability, speeling rat cage,body of rat leaned side,lower limbs were abduction,adduction of lower limbs was hardly,walking and skipping was gammy,facial paralysis indicated,the left eye was smaller than right one,the mice could not roll the body and just shake when the tails were raised and the left spermary was shrink.The scores of motor function of stroke sequela group rats(6.00±0.18) was obviously higher than that of acute stroke group rats(4.33±1.67)(P< 0.01), In comparison of structure of neurons synapse in brain tissue of control group rats and acute stroke group rats,the density of synapse in stroke seguela group rats(8.33±0.91) was significantly increased(P< 0.05), the interspace of the synapse[(10.13±0.56) nm] was narrower(P< 0.05),the synapse length of the active area[(127.12±10.38) nm] was significantly longer(P< 0.05) and the dense material of postsynapse[(76.78±3.45) nm] was thicker in ischemic area(P< 0.05),but there were no dominant changes in hippcampus(P >0.05). CONCLUSION:In a period of the stroke sequela,motor function of rats is gradually restored,the dense of synapse is significantly increased,the interspace of the synapse is narrowed,the length of the active area of synapse is prdonged and the dense material of postsynapse is thickened in ischemic area,which are the foundations of function restoring, and it is as one of vital differentiations as compared with acute stroke.
作者 刘宁平 彭康
出处 《中国临床康复》 CSCD 北大核心 2005年第5期117-119,共3页 Chinese Journal of Clinical Rehabilitation
  • 相关文献

参考文献8

二级参考文献43

  • 1李泓.血浆TXA_2、PGI_2水平与血瘀证及活血化瘀研究[J].中国中西医结合杂志,1995,15(11):701-704. 被引量:81
  • 2颜德馨,胡泉林,王平平,周晓燕,宓哲伟,周良彦.气虚血瘀是人体衰老的主要机制[J].中国医药学报,1989,4(2):10-12. 被引量:114
  • 3周勇,严宣佐,徐音,陶君悌,张丽,顾立刚,刘宏阳.参芪注射液对气虚证小鼠免疫反应影响的实验研究[J].中西医结合杂志,1989,9(5):286-288. 被引量:21
  • 4张洪 魏之玉 等.气虚血瘀在心脑血管疾病及衰老机制中位置[J].山东中医学院学报,1996,20(5):107-108.
  • 5余小骊 龚琼模 等.中风宁1号注射液治疗急性缺血性中风的临床和实验研究[J].中国中西医结合杂志,1994,14(1):34-34.
  • 6[5]Ziv NE, Garner CC. Principles of glutamatergic synapse formation: seemg the forest for the trees. Curr Opin Neurobiol 2001; 11(5):536 -43
  • 7[6]Ahmari SE, Smith SJ. Knowing a nacent synapse when you see it. Neuron 2002; 34(3):333 -6
  • 8[7]Fiala JC, Feinberg M, Popov V, Harris KM. Synaptogenesis via dendritic filopodia in developing hippocampal area CA1. J Neurosci 1998; 18(21): 8900 - 11
  • 9[8]Cline HT.Dendritic arbor development and synaptogenesis. Curr Opin Neurobiol 2001;11(1): 118 -26
  • 10[9]Rao A, Cha EM, Craig AM. Mismatched appositions of prsynaptic and postsynaptic components in isolated hippocampal neurons. J Neurosci 2000; 20(22):8344 - 53

共引文献82

同被引文献34

引证文献2

二级引证文献13

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部