Surgical animal models of heart failure related to coronary heart disease

Abstract

Coronary heart disease is caused by atherosclerotic narrowing of coronary arteries. It accounts for about two-thirds of heart failure cases, which are frequently secondary to myocardial infarction. Despite considerable progress in the understanding and management of heart failure, its incidence, prevalence and economic burden are steadily increasing. Therefore, efficient preventive and therapeutic measures are urgently needed. In order to investigate the mechanisms involved in the pathogenesis of coronary heart disease-related heart failure and to develop therapies, appropriate animal models are indispensable. According to the aetiology of this disorder, surgical models are based on various methods allowing for the narrowing or occlusion of coronary arteries. Depending on the duration and extent of the impairment of coronary blood flow and its consequences for cardiac tissue, these are classified as models of myocardial infarction, cardiac ischemia/reperfusion injury, or chronic cardiac ischemia. In addition, factors such as species, strain, and gender of the laboratory animals also significantly contribute to the pathophysiology of the induced disorder and, therefore, have to be taken into consideration thoroughly when an animal model is to be established.

Infarto do miocárdio experimental em ratos: análise do modelo

“…Another aspect is that due to the rat metabolism characteristics, the phases involved in the infarction evolution such as necrosis, healing and remodeling occur rapidly, which decreases the time of study observation. Finally, the morphological and functional alterations caused by the infarction are similar to those found in humans 8,9 .…”

Reduced N‐Type Ca 2+ Channels in Atrioventricular Ganglion Neurons Are Involved in Ventricular Arrhythmogenesis

“…Before performing reverse‐phase protein microarray, therefore, we used the rat brain as a Ca v 2.2‐α–positive sample and the gastrocnemius muscle as a Ca v 2.2‐α–negative sample to evaluate target specificity of Ca v 2.2‐α antibody (Figure 2). Additionally, we do realize a possible limitation of small animals for extrapolating the findings obtained in this study to humans, although the rat has contributed markedly to assessment of the pathophysiology and treatment of CHF and to the advancement of clinical care 53, 54, 55. Large animals could be an appropriate alternative for translational experiments.…”

Normothermic Cardiac Arrest and Cardiopulmonary Resuscitation: A Mouse Model of Ischemia-Reperfusion Injury

“…7-9,9,10 Models which employ focal ischemia have repeatedly demonstrated results which do not translate to the clinical setting, and larger animal models which allow for whole body hypoperfusion lack access to the full toolset of genetic manipulation possible in the mouse. 11,12 However, in recent years a mouse model of cardiac arrest and cardiopulmonary resuscitation has emerged which can be adapted to model AKI. 13 This model reliably reproduces physiologic, functional, anatomic, and histologic outcomes seen in clinical AKI, is rapidly repeatable, and offers all of the significant advantages of a murine surgical model, including access to genetic manipulative techniques, low cost relative to large animals, and ease of use.…”