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Updated: Jul 13, 2025
A Murine Closed-chest Model of Myocardial Ischemia and Reperfusion
Published on: July 17, 2012
Evaluation of time-dependent phenotypes of myocardial ischemia-reperfusion in mice
Xiang-Min Meng1, Jing-Han Yuan1, Zhen-Fang Zhou1
1Regenerative Medicine Research Center, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
Background:
A mouse model of myocardial ischemia-reperfusion (I/R) is widely used to study myocardial ischemia-reperfusion injury (I/RI). However, few studies focus on the direct comparison of the extent of pathological events resulting from variant durations of ischemia and reperfusion process.
Methods:
A mouse model of I/RI was established by ligation and perfusion of the left anterior descending coronary artery (LAD), and the dynamic changes were recorded by electrocardiogram at different stages of I/R. Subsequently, reperfusion duration was used as a variable to directly compare the phenotypes of different myocardial injury degrees induced by 3 h, 6 h and 24 h reperfusion from myocardial infarct size, myocardial apoptosis, myocardial enzyme, and inflammatory cytokine levels.
Results:
All mice subjected to myocardial I/R surgery showed obvious myocardial infarction, extensive myocardial apoptosis, dynamic changes in serum myocardial enzyme and inflammatory cytokines, at least for the first 24 h of reperfusion. The infarct size and apoptosis rates gradually increased with the extension of reperfusion time. The peaks of serum myocardial enzyme and inflammatory cytokines occurred at 6 h and 3 h of reperfusion, respectively. We also established I/R mice models with 30 and 60 mins of ischemia. After 21 days of remodeling, longer periods of ischemia increased the degree of fibrosis and reduced cardiac function.
Conclusions:
In summary, we conclude that reperfusion durations of 3 h, 6 h, and 24 h induces different injury phenotypes in ischemia-reperfusion mouse model. At the same time, the ischemia duration before reperfusion also affects the degree of cardiac remodeling.
Insights
Investigating myocardial ischemia-reperfusion (I/R) injury in mice reveals that varying reperfusion times (3, 6, 24 hours) create distinct injury patterns. Longer ischemia durations also worsen cardiac remodeling and function.
Area of Science:
- Cardiovascular Research
- Pathology
- Animal Models
Background:
- Myocardial ischemia-reperfusion (I/R) injury is a critical area of cardiovascular research.
- Existing mouse models of I/R injury lack direct comparisons of pathological events across varied ischemia and reperfusion durations.
- Understanding these variations is crucial for developing targeted therapeutic strategies.
Purpose of the Study:
- To directly compare the pathological consequences of different reperfusion durations (3, 6, and 24 hours) on myocardial injury in a mouse model.
- To investigate the impact of varying ischemia durations (30 and 60 minutes) on cardiac remodeling and function post-reperfusion.
Main Methods:
- Established a mouse model of myocardial I/R using left anterior descending coronary artery ligation and reperfusion.
- Monitored dynamic electrocardiogram changes during I/R.
- Assessed myocardial infarct size, apoptosis, serum enzyme levels, and inflammatory cytokines at different reperfusion times.
- Evaluated cardiac fibrosis and function after 21 days of remodeling in models with varied ischemia durations.
Main Results:
- Myocardial I/R induced infarction, apoptosis, and altered serum markers within 24 hours.
- Infarct size and apoptosis rates increased with longer reperfusion times.
- Serum myocardial enzyme and inflammatory cytokine levels peaked at 6 and 3 hours of reperfusion, respectively.
- Extended ischemia durations (30-60 minutes) led to increased fibrosis and reduced cardiac function post-remodeling.
Conclusions:
- Reperfusion durations of 3, 6, and 24 hours elicit distinct myocardial injury phenotypes in the I/R mouse model.
- Ischemia duration significantly influences the extent of cardiac remodeling and functional decline following reperfusion.
