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兔舒张性心力衰竭模型的建立 被引量:13

Rabbit model of diastolic heart failure
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摘要 探索建立兔舒张性心力衰竭 (DHF)模型的方法。采用腹主动脉缩窄法建立兔压力负荷性心肌肥厚模型 ,通过超声心动图监测和左心导管检查测定左室舒张末压和松弛时间常数。结果显示腹主动脉内径减少 40 %~ 5 0 %的实验兔术后 8周室间隔和左室后壁明显增厚 ,左室舒张末压明显升高 ,松弛时间常数明显延长 ;电镜下可见其肌原纤维排列紊乱 ,肌节结构模糊 ,闰盘结构不连续、模糊 ,线粒体数量明显增多 ,丛状聚集 ,肌浆网肿胀、破裂 ,数目减少。结论为本研究成功地建立了DHF动物模型 ,为进一步研究DHF的发病机制。 To establish rabbit model of diastolic heart failure for experimental use. The animal model was made in rabbits by abdominal aortic coarctation. Systolic and diastolic functions were assessed by echocardiography and catheterization during left hypertrophy progression. Ultrastructural changes of rabbit left ventricle tissue were observed by scanning electron microscopy. In rabbits with reduced diameter of abdominal aorta to approximately 40%~50% of their original size, the interventricular septum and left ventricular posterior wall thickness were significantly increased. Moreover, myocardial relaxation was prolonged and left ventricular end diastolic pressures were significant increased in these rabbits after 8 weeks obtained through cardiac catheterization, despite normal left ventricular systolic function. Remarkable changes of these rabbits in intracellular membranous ultrastructures such as nucleus, mitochondria and sarcoplasmic reticulum were observed by scanning electron microscopy. Myocardial fiber disarray was evident, where the fibers run in various directions. Mitochondria clustered with wavy form. Sarcoplasmic reticulum network density decreased. It is suggesting that rabbit model of DHF was established successfully. It is important to establish DHF model to pathogenesis research, diagnosis and treatment of DHF.
出处 《基础医学与临床》 CSCD 北大核心 2001年第4期379-382,共4页 Basic and Clinical Medicine
基金 国家自然科学基金 (39970 2 94)
关键词 舒张性心力衰竭 模型 解剖结构 血流动力学 心肌组织 animal model diastolic heart failure
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参考文献4

  • 1[1]Vasan RS, Levy D. Defining diastolic heart failure: a call for standardized diagnostic creteria[J]. Circulation, 2000,101:2118-2121.
  • 2[2]Heller LJ, Opsahl JA, Wernsing SE, et al. Myocardial and plasma renin-angiotensinogen dynamics during pressure-induced cardiac hypertrophy[J]. Am J Physiol, 1998,274:R849-856.
  • 3[3]Litten RZ, Martin BJ, Low RB, et al. Altered myosin isozyme pattern from pressure-overloaded and thyrotoxic hypertrophied rabbit hearts[J]. Circ Res, 1982, 50:856-864.
  • 4[4]Lenihan DJ, Gerson MC, Hoit BD, et al. Mechanisms, diagnosis, and treatment of diastolic heart failure[J]. Am Heart J, 1995,130:153-166.

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