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Myocardial infarction and cardiac remodelling in mice

Published online by Cambridge University Press:  21 August 2002

Fang Yang ,
Yun-He Liu ,
Xiao-Ping Yang ,
Jiang Xu ,
Alissa Kapke  and
Oscar A. Carretero
Fang Yang
Affiliation:
Hypertension and Vascular Research Division, Department of Internal Medicine and Division of Biostatistics and Research Epidemiology, Henry Ford Hospital, Detroit, MI, USA
Yun-He Liu
Affiliation:
Hypertension and Vascular Research Division, Department of Internal Medicine and Division of Biostatistics and Research Epidemiology, Henry Ford Hospital, Detroit, MI, USA
Xiao-Ping Yang
Affiliation:
Hypertension and Vascular Research Division, Department of Internal Medicine and Division of Biostatistics and Research Epidemiology, Henry Ford Hospital, Detroit, MI, USA
Jiang Xu
Affiliation:
Hypertension and Vascular Research Division, Department of Internal Medicine and Division of Biostatistics and Research Epidemiology, Henry Ford Hospital, Detroit, MI, USA
Alissa Kapke
Affiliation:
Hypertension and Vascular Research Division, Department of Internal Medicine and Division of Biostatistics and Research Epidemiology, Henry Ford Hospital, Detroit, MI, USA
Oscar A. Carretero
Affiliation:
Hypertension and Vascular Research Division, Department of Internal Medicine and Division of Biostatistics and Research Epidemiology, Henry Ford Hospital, Detroit, MI, USA
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Abstract

We established a mouse model of cardiac dysfunction due to myocardial infarction (MI). For this we ligated the left anterior descending coronary artery in male C57BL/6J mice and assessed healing and left ventricular (LV) remodelling at 1, 2 and 4 days and 1, 2 and 4 weeks after MI. Echocardiography was performed at 1 and 2 weeks and 1, 2, 4 and 6 months after MI. We found that neutrophil infiltration of the infarct border was noticeable at 1-2 days. Marked macrophage infiltration occurred at day 4, while lymphocyte infiltration was apparent at 7-14 days. Massive proliferation of fibroblasts and collagen accumulation began by day 7-14, and scar formation was completed by day 21. LV diastolic dimension increased markedly at 2 weeks and remained at the same level thereafter. LV shortening fraction decreased significantly at 2 weeks and then slowly decreased. In non-infarcted areas of the LV, myocyte cross-sectional area and interstitial collagen fraction increased progressively, reaching a maximum at 4 months. This study provides important qualitative and quantitative information about the natural history of cardiac remodelling after MI in mice. Experimental Physiology (2002) 87.5, 547-555.

Type
Full Length Papers
Information
Experimental Physiology , Volume 87 , Issue 5 , September 2002 , pp. 547 - 555
Copyright
© The Physiological Society 2002

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