Related Experiment Video
Updated: Jun 27, 2026
Permanent Ligation of the Left Anterior Descending Coronary Artery in Mice: A Model of Post-myocardial Infarction Remodelling and Heart Failure
Published on: December 2, 2014
Time-dependent changes of myocardial and systemic oxidative stress are dissociated after myocardial infarction
Takahiro Inoue1, Tomomi Ide, Mayumi Yamato
1Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Abstract:
Reactive oxygen species (ROS) is increased in myocardium after myocardial infarction (MI), which may play a causal role in cardiac remodelling. However, there is scant direct and longitudinal evidence that systemic oxidative stress is enhanced accompanying an increase of ROS in myocardium. The authors conducted a comprehensive investigation of ROS markers by simultaneously sampling urine, blood and myocardium and in vivo ESR for the heart at different stages of post-MI cardiac remodelling in mouse with permanent occlusion of left coronary artery. Systemic oxidative markers increased at early days after MI and were normalized later. In contrast, TBARS and 4-hexanoyl-Lys staining were increased in non-infarct myocardium at day 28. The enhancement of ESR signal decay of methoxycarbonyl-PROXYL measured at the chest was associated with the progression of left ventricle dilatation and dysfunction. This study provided the direct evidence that redox alteration and production of ROS occurred in myocardium during the progression of cardiac remodelling and failure; however, ROS marker levels in blood and urine do not reflect the production of ROS from failing myocardium.
Insights
Following myocardial infarction (MI), cardiac reactive oxygen species (ROS) increase, but systemic markers in blood and urine do not reflect this. Myocardial ROS production is confirmed during cardiac remodelling and failure.
Area of Science:
- Cardiovascular Research
- Oxidative Stress Biology
Background:
- Reactive oxygen species (ROS) are implicated in cardiac remodelling post-myocardial infarction (MI).
- Limited longitudinal data exists on systemic oxidative stress correlating with myocardial ROS in heart failure.
Purpose of the Study:
- To investigate systemic and myocardial oxidative stress markers during post-MI cardiac remodelling.
- To determine if systemic ROS markers reflect myocardial ROS production in failing hearts.
Main Methods:
- Mice underwent permanent left coronary artery occlusion to model MI.
- Simultaneous sampling of urine, blood, and myocardium for ROS markers.
- In vivo Electron Spin Resonance (ESR) used to measure cardiac ROS.
Main Results:
- Systemic oxidative markers peaked early post-MI and normalized later.
- Increased TBARS and 4-hexanoyl-Lys staining observed in non-infarct myocardium at day 28.
- Enhanced ESR signal decay correlated with left ventricle dilatation and dysfunction.
- Myocardial ROS production increased during cardiac remodelling and failure.
Conclusions:
- Direct evidence confirms redox alterations and ROS production in the myocardium during cardiac remodelling and failure.
- Systemic ROS markers in blood and urine are unreliable indicators of myocardial ROS production in heart failure.
Related Concept Videos
01:21Myocarditis I: Introduction
01:20Blood Studies for Cardiovascular System I: Cardiac Biomarkers
The essential diagnostic tools for detecting myocardial necrosis and monitoring individuals suspected of having acute coronary syndrome (ACS) include:
Troponins
Troponins, particularly cardiac troponins I and T, are the most precise and sensitive markers of myocardial injury. They are detectable within 4-6 hours of myocardial injury and remain...
01:29Pathophysiology of Cardiac Performance
01:19Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations