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心肌缺血再灌注损伤大鼠冠状微循环改变的实验研究 被引量:16

Study on the Coronary Microcirculation Resisting in Cardial Ischemia Reperfusion Injury in Rats
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摘要 目的研究心肌缺血再灌注损伤大鼠冠状微循环变化的特点及与影响因素的关系。方法对心肌缺血再灌注损伤 (CIRI)大鼠模型、心肌缺血 (MCI)大鼠模型和假手术后大鼠3组的心肌毛细血管墨汁灌流数、大鼠冠状微循环荧光变化时间及心肌组织丙二醛 (MDA)、心肌组织一氧化氮 (NO)含量、心肌组织钠 -钾 -ATP酶 (Na + -K + -ATPase)、心肌组织钙 -ATP酶 (Ca2 + -ATPase)、血清肌酸激酶 (CK)活性、血浆血栓素B2(TXB 2)和血浆6-酮 -前列环素F1α(6 -K -PGF1α)含量进行检测和相关分析。结果较之MCI模型组和假手术后组 ,①CIRI模型组大鼠右室前壁外层、左室前壁中内层、室间隔前2/3部位毛细血管灌流数均明显减少 ;心脏表面荧光出现时间 (AT)、密布时间 (FT)和饱和时间 (ST)均延长 (均P<0.05或<0.01)。②CIRI模型组大鼠心肌组织MDA含量明显增高,而NO含量减少 ;血浆6 -K -PGF1α含量下降 ,而TXB2 含量显著升高 ;Na + -K + -ATPase和Ca2 + -ATPase活性均降低 ,而血清CK水平升高(均P<0.05或<0.01)。③CIRI模型组大鼠心脏左室前壁中内层毛细血管墨汁灌流数与MDA、NO、TXB2、6 -K -PGF1α、Ca2 + -ATPase、CK等6项指标的变化都有相关关系 (均P<0.05或<0.01) ,与这6项指标的阳性率亦相同 (均P>0.05)。 Objective To study the feature of the coronary microcirculation change to the cardial ischemia reperfusion injury(CIRI)and relationship of influence factor.Methods Three groups are as follows:the CIRI model of living rats,myocardial injury(MCI)model of living rats and healthy living rats,we detected the number of myocardial capillary perfused with ink,the change time of living rat's fluorescence in coronary microcirculation,the content of maloncliddehyde(MDA)and the nitric oxide(NO)in the cardiac muscle,the vitality of Na + -k + -ATPase,Ca 2+ -ATPase in the cardiac muscle and creatine kinase(CK)in the serum,and the content of the TXB 2 and6-k-PGF 1α in the plasma,and do relative analysis.Results By comparing with MCI model group and healthy control group,the results are as follows:①In the CIRI model group,the number of capillary perfused in outer layer of ventriculus dexter's fore-wall,mid-inner layer of ventriculus sinister's fore-wall and septum intervenˉtriculare's frontal two-third place decreased greatly.In heart's surface,the fluorescence-appearing time(AT),the fluorescence-high-density time and saturated time(ST)are longer(P<0.05or P<0.01).②In the CIRI living rats model group,the content of MDA in the cardiac muscle increased greatly,but the content of the nitric oxide(NO)in the cardiac muscle decreased,6-K-PGF 1α content in the plasma decreased.However,the TXB 2 content in the plasma increased greatly,the vitality of Na + -K + -ATPase and Ca 2+ -ATPase decreased,but the level of CK in the serum rose(P<0.05or P<0.01)③In the CIRI living rats model group,the number of capilˉlary perfused with ink in the mid-inner layer of ventriculus sinister's fore-wall is relatde to the change of six indexˉes:MDA,NO,TXB 2 ,6-K-PGF 1α ,Ca 2+ -ATPase and CK(P<0.05or P<0.01),and it is the same as the positive rate of the six indexes(P>0.05).Conclusions The coronary microcirculation resisting is an imporˉtant pathologic and physiologic link to the CIRI's formation.Its formation is related to a few mechanisms:Oxygen free radical increasing,calcium overloading,the blood-vessel endothelial cell's function being evidently injured.
出处 《中国微循环》 2004年第4期204-208,共5页 Journal of Chinese Microcirculation
基金 湖南省教育厅科研基金资助项目(97B082)
关键词 缺血再灌注损伤 心脏 冠状微循环 Ischemial reperfusion injury Heart Coronary microcirculation
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参考文献11

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二级参考文献14

  • 1袁肇凯,黄献平,曹金枝,胡志希,简亚平.心肌缺血再灌注损伤大鼠冠状微循环改变的实验研究[J].中国微循环,2004,8(4):204-208. 被引量:16
  • 2裴建明,李红梅,牛国保,朱妙章,高峰,臧益民,施溥涛.降钙素基因相关肽和心房肽对犬冠脉的舒张作用[J].中国应用生理学杂志,1995,11(1):47-50. 被引量:4
  • 3裴建明,李红梅,牛国保,朱妙章,臧益民,王跃民,张宁仔,施溥涛,蓝中.降钙素基因相关肽对心肌缺血时心脏功能的影响[J].心功能杂志,1996,8(3):140-144. 被引量:5
  • 4Eisner DA,Trafford AW,Diaz ME,et al.The control of carelease from the cardiac sarcoplasmic reticulum:regulation versus autoregulation[J].Cardiovascular Research.1998,38:589~604
  • 5Derek M Yellon,Gary F Baxter,David Garado-Dorado,et al.Ischaemic preconditioning:present position and future directions[J].Cardiovascular Research.1998,37:21~33
  • 6施新猷.急性心肌缺血模型的复制[A].见:施新猷主编.医学动物实验方法[M].北京:人民卫生出版社,1986.237-238.
  • 7田牛.微循环形态学研究方法[A].见:田牛.微循环[M].北京:科学出版社,1986.8-9.
  • 8陶恭明 金惠铭 见陈文杰 田牛 赵国忠主编.荧光血管造影法及其在微循环研究中的应用[A].见陈文杰,田牛,赵国忠主编.微循环的理论和应用[M].北京:人民卫生出版社,1987.293-303.
  • 9吴其夏.体液因素和血液循环病理生理学[M].北京:北京医科大学协和医科大学联合出版社,1992.289-292.
  • 10Steurer G,Yang P,Rao V,et al.Acute myoccardial infarction,reperfusion injury,and intravenous magnesium therapy; basic concepts and clinical implications[J].Am Heart J.1996,132(2pt 2 Su):478~482

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