Myocardial infarction in the C57BL/6J mouse - A quantifiable and highly reproducible experimental model
Myocardial infarction in the C57BL/6J mouse - A quantifiable and highly reproducible experimental model
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DOI：
10.1016/s1054-8807(03)00129-7
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发表时间：
2004-03-01
影响因子：
3.7
通讯作者：
Lim, SK
中科院分区：
文献类型：
--
作者：
Salto-Tellez, M;Lim, SY;Lim, SK
简介：实验室小鼠是心血管研究的有力工具。在本报告中，我们描述了一种可重复的小鼠心肌梗死模型的方法，该方法将允许对分子和病理生理学变量进行后续的比较和定量研究。方法：（A）通过主动脉灌注乳胶染料或荧光珠来绘制C57BL/6J小鼠（n=20）左心室中主要冠状动脉（包括间隔动脉）的分布。 (B) 对结扎左前降支 (LAD) 冠状动脉最近端后的心肌梗塞区域进行量化。 (C) 分析不同时间点与梗塞平行的组织学变化的一致性。结果：(A) 小鼠的冠状动脉树与人类不同，特别是在隔膜的血液供应方面。 (B) 与之前的看法相反，小鼠的间隔冠状动脉的起源是可变的。 (C) 紧邻左耳平面下方的 LAD 持续结扎可确保梗死面积具有统计显着性、可重复性。 (D)可以以类似于人类所描述的方式在组织学水平上监测缺血性变化。结论：我们阐述了一种在小鼠模型中实现实验性急性心肌梗死最大重现性的方法，因为左心室下半部的灌注持续丧失。这将允许在受控和可量化的实验模型环境中研究分子和生理变量。 (C) 2004 Elsevier Inc. 保留所有权利。
Introduction: The laboratory mouse is a powerful tool in cardiovascular research. In this report, we describe a method for a reproducible mouse myocardial infarction model that would allow subsequent comparative and quantitative studies on molecular and pathophysiological variables. Methods: (A) The distribution of the major coronary arteries including the septal artery in the left ventricle of the C57BL/6J mice (n=20) was mapped by perfusion of latex dye or fluorescent beads through the aorta. (B) The territory of myocardial infarction after the ligation of the most proximal aspect of the left anterior descending (LAD) coronary artery was quantified. (C) The consistency in the histological changes parallel to the infarction at different time points was analyzed. Results: (A) The coronary artery tree of the mouse is different from human and, particularly, in regard to the blood supply of the septum. (B) Contrary to previous belief, the septal coronary artery in the mouse is variable in origin. (C) A constant ligation of the LAD immediately below the left auricular level ensures a statistically significant reproducible infarct size. (D) The ischemic changes can be monitored at a histological level in a way similar to what is described in the human. Conclusion: We illustrate a method for maximal reproducibility of experimental acute myocardial infarction in the mouse model, due to a consistent loss of perfusion in the lower half of the left ventricle. This will allow the study of molecular and physiological variables in a controlled and quantifiable experimental model environment. (C) 2004 Elsevier Inc. All rights reserved.