Rat infarct model of myocardial infarction and heart failure.
Rat infarct model of myocardial infarction and heart failure.
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DOI：
10.1016/1071-9164(95)90019-5
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发表时间：
1995-03-01
影响因子：
6
通讯作者：
Raya, T E
中科院分区：
文献类型：
--
作者：
Goldman, S;Raya, T E
本综述概述了大鼠冠状动脉结扎心力衰竭模型的发展和当前使用。描述了结扎左冠状动脉和获得形态/血流动力学测量的技术。作者展示了该模型中观察到的病理学与临床缺血性心脏病的关系。在整个审查过程中，我们努力将该模型中发生的变化与临床相关观察结果联系起来。例如，这些大鼠心力衰竭的进展类似于患者遭受大面积心肌梗塞后存活下来，但在没有再次缺血性损伤的情况下继续发展为心力衰竭的情况。在患有大面积梗塞的大鼠和人中，即使在梗塞时未受损，未梗塞的心肌也无法充分补偿以防止最终发展为心力衰竭。除了很好地近似人类疾病之外，大鼠对药物干预（如血管紧张素转换酶抑制剂）的反应已被证明有助于预测人类接受相同治疗后会发生什么。关于心室重塑分子控制的更多最新数据强调了该模型如何通过检查同一组织中的生化、药理学和生理变化，为综合生理学研究提供重要信息。
This review outlines the development and current use of the rat coronary artery ligation model of heart failure. The techniques to ligate the left coronary artery and to obtain morphologic/hemodynamic measurements are described. The authors show how the pathology seen in this model relates to clinical ischemic heart disease. An effort is made throughout the review to relate the changes that occur in this model to clinically relevant observations. For example, the progression to heart failure in these rats is similar to what happens when a patient sustains a large myocardial infarction, survives, but goes on to develop heart failure without another ischemic insult. In both rats and people with large infarctions, the noninfarcted myocardium, even though not damaged at the time of the infarct, cannot compensate sufficiently to prevent the eventual development of heart failure. In addition to being a good approximation of human disease, the responses to pharmacologic interventions, like angiotensin converting enzyme inhibitors, in rats has proved useful in predicting what will happen in humans given the same treatment. More recent data on the molecular control of ventricular remodeling emphasizes how this model will provide important information in the study of integrated physiology by examining biochemical, pharmacologic, and physiologic changes in the same tissue.