Animal Models of Cardiovascular Disease

被引:28
作者
Chorro, Francisco J. [1 ]
Such-Belenguer, Luis [1 ]
Lopez-Merino, Vicente [1 ]
机构
[1] Univ Valencia, Serv Cardiol, Hosp Clin Univ, Dept Med & Fisiol, Valencia 46010, Spain
来源
REVISTA ESPANOLA DE CARDIOLOGIA | 2009年 / 62卷 / 01期
关键词
Cardiovascular research; Preclinical research; Animal models; APOLIPOPROTEIN-A-I; PIG VENTRICULAR MYOCYTES; DIRECTED GENE-TRANSFER; ATRIAL-FIBRILLATION; MOUSE MODELS; MITOCHONDRIAL-MEMBRANE; MYOCARDIAL-ISCHEMIA; STRUCTURAL-CHANGES; SURGICAL-TREATMENT; DEFICIENT MICE;
D O I
10.1016/S0300-8932(09)70023-5
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The use of animal models to study cardiovascular disease has made a substantial contribution to increasing our understanding of disease pathogenesis, has led to the development of diagnostic techniques, and has made it possible to verify the effectiveness of different preventative and therapeutic approaches, whether pharmacological or interventional. The main limitations stem from differences between human and experimentally induced pathology, in terms of both genetic regulatory mechanisms and factors that influence cardiovascular function. The experimental models and preparations used in cardiovascular research include those based on isolated cells or tissues or structures immersed in organ baths. The Langendorff system enables isolated perfused hearts to be studied directly under conditions of either no load or controlled loading. In small mammals, a number of models have been developed of cardiovascular conditions that result from spontaneous genetic mutations or, alternatively, that may be induced by specific genomic modification. One of the techniques employed is gene transfer, which can involve the controlled induction of mutations that result in the expression of abnormalities associated with the development of a broad range of different types of cardiovascular disease. Larger animals are used in experimental models in which it is important that physiological regulatory and homeostatic mechanisms are present.
引用
收藏
页码:69 / 84
页数:16
相关论文
共 110 条
  • [61] CHRONICALLY IMPLANTED SYSTEM FOR AUTOMATIC DEFIBRILLATION IN ACTIVE CONSCIOUS DOGS - EXPERIMENTAL-MODEL FOR TREATMENT OF SUDDEN-DEATH FROM VENTRICULAR-FIBRILLATION
    MIROWSKI, M
    MOWER, MM
    LANGER, A
    HEILMAN, MS
    SCHREIBMAN, J
    [J]. CIRCULATION, 1978, 58 (01) : 90 - 94
  • [62] INTRAVENOUS-INJECTION OF RABBIT APOLIPOPROTEIN-A-I INHIBITS THE PROGRESSION OF ATHEROSCLEROSIS IN CHOLESTEROL-FED RABBITS
    MIYAZAKI, A
    SAKUMA, S
    MORIKAWA, W
    TAKIUE, T
    MIAKE, F
    TERANO, T
    SAKAI, M
    HAKAMATA, H
    SAKAMOTO, YI
    NAITO, M
    RUAN, YM
    TAKAHASHI, K
    OHTA, T
    HORIUCHI, S
    [J]. ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1995, 15 (11) : 1882 - 1888
  • [63] Effect of remodelling, stretch and ischaemia on ventricular fibrillation frequency and dynamics in a heart failure model
    Moreno, J
    Zaitsev, AV
    Warren, M
    Berenfeld, O
    Kalifa, J
    Lucca, E
    Mironov, S
    Guha, P
    Jalife, J
    [J]. CARDIOVASCULAR RESEARCH, 2005, 65 (01) : 158 - 166
  • [64] CHRONIC RAPID ATRIAL-PACING - STRUCTURAL, FUNCTIONAL, AND ELECTROPHYSIOLOGICAL CHARACTERISTICS OF A NEW MODEL OF SUSTAINED ATRIAL-FIBRILLATION
    MORILLO, CA
    KLEIN, GJ
    JONES, DL
    GUIRAUDON, CM
    [J]. CIRCULATION, 1995, 91 (05) : 1588 - 1595
  • [65] PRECONDITIONING WITH ISCHEMIA - A DELAY OF LETHAL CELL INJURY IN ISCHEMIC MYOCARDIUM
    MURRY, CE
    JENNINGS, RB
    REIMER, KA
    [J]. CIRCULATION, 1986, 74 (05) : 1124 - 1136
  • [66] Mechanisms of atrial fibrillation: Lessons from animal models
    Nattel, S
    Shiroshita-Takeshita, A
    Brundel, BJJM
    Rivard, L
    [J]. PROGRESS IN CARDIOVASCULAR DISEASES, 2005, 48 (01) : 9 - 28
  • [67] Knockin animal models of inherited arrhythmogenic diseases:: What have we learned from them?
    Nilles, Kathy M.
    London, Barry
    [J]. JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, 2007, 18 (10) : 1117 - 1125
  • [68] Reactive oxygen species as mediators of signal transduction in ischemic preconditioning
    Otani, H
    [J]. ANTIOXIDANTS & REDOX SIGNALING, 2004, 6 (02) : 449 - 469
  • [69] Electrophysiological effects of CI-980, a tubulin binding agent, on guinea-pig papillary muscles
    Perez, O
    Valenzuela, C
    Delpon, E
    Tamargo, J
    [J]. BRITISH JOURNAL OF PHARMACOLOGY, 1997, 120 (02) : 187 - 192
  • [70] SEVERE HYPERCHOLESTEROLEMIA AND ATHEROSCLEROSIS IN APOLIPOPROTEIN-E-DEFICIENT MICE CREATED BY HOMOLOGOUS RECOMBINATION IN ES CELLS
    PLUMP, AS
    SMITH, JD
    HAYEK, T
    AALTOSETALA, K
    WALSH, A
    VERSTUYFT, JG
    RUBIN, EM
    BRESLOW, JL
    [J]. CELL, 1992, 71 (02) : 343 - 353