Please use this identifier to cite or link to this item: https://doi.org/10.1016/S1054-8807(03)00129-7
Title: Myocardial infarction in the C57BL/6J mouse: A quantifiable and highly reproducible experimental model
Authors: Salto-Tellez, M. 
Lim, S.Y.
El, Oakley R.M. 
Tang, T.P.L.
Almsherqi, Z.A.M. 
Lim, S.-K.
Keywords: C57BL/6J mouse model
Myocardial infarction
Reproducibility
Issue Date: 2004
Source: Salto-Tellez, M.,Lim, S.Y.,El, Oakley R.M.,Tang, T.P.L.,Almsherqi, Z.A.M.,Lim, S.-K. (2004). Myocardial infarction in the C57BL/6J mouse: A quantifiable and highly reproducible experimental model. Cardiovascular Pathology 13 (2) : 91-97. ScholarBank@NUS Repository. https://doi.org/10.1016/S1054-8807(03)00129-7
Abstract: 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. © 2004 Elsevier Inc. All rights reserved.
Source Title: Cardiovascular Pathology
URI: http://scholarbank.nus.edu.sg/handle/10635/30501
ISSN: 10548807
DOI: 10.1016/S1054-8807(03)00129-7
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