Animal models of heart failure

被引:8
作者
Arnolda, LF [1 ]
Llewellyn-Smith, IJ
Minson, JB
机构
[1] Flinders Univ S Australia, Ctr Neurosci, Bedford Pk, SA 5042, Australia
[2] Flinders Univ S Australia, Cardiovasc Neurosci Grp, Bedford Pk, SA 5042, Australia
来源
AUSTRALIAN AND NEW ZEALAND JOURNAL OF MEDICINE | 1999年 / 29卷 / 03期
关键词
myocardial infarction; doxorubicin cardiomyopathy; pacing-induced heart failure; sympathetic nervous system; renin; vasopressin;
D O I
10.1111/j.1445-5994.1999.tb00735.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Animal models of heart failure present homogenous groups of animals all with heart failure produced by a well defined lesion at a particular stage of evolution, in contrast to humans, who present with hears failure of uncertain duration front a wide variety of causes and with marked variation in age and pre-morbid health and fitness. Animal models of heart failure provide diseased groups of animals in which experimental procedures, not possible in humans, can be evaluated and in which new treatments can be tested before their safety is established in humans. An ideal model should have a common human counterpart and should closely mimic heart failure in humans. Thus the haemodynamic changes should include increased cardiac filling pressures and law cardiac output There should be evidence of activation of the sympathetic nervous system and increased secretion of hormones such as renin, angiotensin, aldosterone, vasopressin, atrial natriuretic factor and endothelin. The clinical features of the human syndrome such as cardiomegaly, lung and peripheral oedema and decreased exercise tolerance should be present. Lastly, the model should be inexpensive and technically simple to produce and study. This paper reviews some commonly used models of heart failure in relation to the criteria listed above. There is no perfect animal model of heart failure and in practice one should match the model to the purpose of the the study.
引用
收藏
页码:403 / 409
页数:7
相关论文
共 49 条
[1]  
ABELMANN WH, 1973, CARDIOMYOPATHIES, P509
[2]   EDEMA OF CARDIAC ORIGIN - STUDIES OF BODY-WATER AND SODIUM, RENAL-FUNCTION, HEMODYNAMIC INDEXES, AND PLASMA HORMONES IN UNTREATED CONGESTIVE CARDIAC-FAILURE [J].
ANAND, IS ;
FERRARI, R ;
KALRA, GS ;
WAHI, PL ;
POOLEWILSON, PA ;
HARRIS, PC .
CIRCULATION, 1989, 80 (02) :299-305
[3]   SPECTRUM AND OUTCOME OF CONGESTIVE-HEART-FAILURE IN A HOSPITALIZED POPULATION [J].
ANDERSSON, B ;
WAAGSTEIN, F .
AMERICAN HEART JOURNAL, 1993, 126 (03) :632-640
[4]   VASOCONSTRICTOR ROLE FOR VASOPRESSIN IN EXPERIMENTAL HEART-FAILURE IN THE RABBIT [J].
ARNOLDA, L ;
MCGRATH, BP ;
COCKS, M ;
JOHNSTON, CI .
JOURNAL OF CLINICAL INVESTIGATION, 1986, 78 (03) :674-679
[5]   SKELETAL-MUSCLE METABOLISM IN HEART-FAILURE IN RATS [J].
ARNOLDA, L ;
BROSNAN, J ;
RAJAGOPALAN, B ;
RADDA, GK .
AMERICAN JOURNAL OF PHYSIOLOGY, 1991, 261 (02) :H434-H442
[6]   ADRIAMYCIN CARDIOMYOPATHY IN THE RABBIT - AN ANIMAL-MODEL OF LOW OUTPUT CARDIAC-FAILURE WITH ACTIVATION OF VASOCONSTRICTOR MECHANISMS [J].
ARNOLDA, L ;
MCGRATH, B ;
COCKS, M ;
SUMITHRAN, E ;
JOHNSTON, C .
CARDIOVASCULAR RESEARCH, 1985, 19 (06) :378-382
[7]   SYSTEMIC AND REGIONAL EFFECTS OF VASOPRESSIN AND ANGIOTENSIN IN ACUTE LEFT-VENTRICULAR FAILURE [J].
ARNOLDA, L ;
MCGRATH, BP ;
JOHNSTON, CI .
AMERICAN JOURNAL OF PHYSIOLOGY, 1991, 260 (02) :H499-H506
[8]   SKELETAL-MUSCLE METABOLISM IN HEART-FAILURE - A P-31 NUCLEAR-MAGNETIC-RESONANCE SPECTROSCOPY STUDY OF LEG MUSCLE [J].
ARNOLDA, L ;
CONWAY, M ;
DOLECKI, M ;
SHARIF, H ;
RAJAGOPALAN, B ;
LEDINGHAM, JGG ;
SLEIGHT, P ;
RADDA, GK .
CLINICAL SCIENCE, 1990, 79 (06) :583-589
[9]   THE SPONTANEOUSLY HYPERTENSIVE RAT AS A MODEL OF THE TRANSITION FROM COMPENSATED LEFT-VENTRICULAR HYPERTROPHY TO FAILURE [J].
BING, OHL ;
BROOKS, WW ;
ROBINSON, KG ;
SLAWSKY, MT ;
HAYES, JA ;
LITWIN, SE ;
SEN, S ;
CONRAD, CH .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1995, 27 (01) :383-396
[10]   A NON-SURGICAL CANINE MODEL OF CHRONIC LEFT-VENTRICULAR MYOCARDIAL DYSFUNCTION [J].
CARLYLE, PF ;
COHN, JN .
AMERICAN JOURNAL OF PHYSIOLOGY, 1983, 244 (06) :H769-H774