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Myocardial ischemia MI/myocardial ischemia-reperfusion animal model

Myocardial ischemia MI/myocardial ischemia-reperfusion animal model

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Myocardial ischemia/myocardial infarction
Cardiovascular disease model

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Model Introduction

Model Introduction

Platform Service Advantages

Platform Service Advantages

Experimental results

Experimental results

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Myocardial ischemia/myocardial infarction

Introduction to MI/MIRI Animal Models

Currently, several methods are available for establishing animal models of myocardial ischemia, including coronary artery ligation, pharmacological induction, balloon occlusion, embolization, and thrombosis. Among these, coronary artery ligation is straightforward to perform, produces a well-defined vascular occlusion, closely mimics the pathophysiological processes underlying myocardial infarction, and facilitates effective translation to clinical settings.

MI/MIRI Animal Model Platform Service Advantages of Aniphe BioLab

The platform boasts mature model‑generation techniques and a standardized quality‑control system, providing comprehensive support for research on myocardial infarction and myocardial ischemia–reperfusion injury, as well as for drug discovery and development.

Comprehensive model coverage

Mature minimally invasive surgical technique

A minimally invasive ligation protocol is employed, eliminating the need for ventilator support; it features minimal trauma, a low rate of postoperative infection, and can be used to establish animal models on a large scale.

Standardization of the modeling process

The model exhibits excellent stability.

The modeling success rate is high, and it can reliably reproduce typical phenotypes such as myocardial infarction, impaired cardiac function, and myocardial injury, with minimal intergroup variability.

Multidimensional Evaluation System

The testing system has been improved.

It supports a range of assays, including cardiac function assessment, infarct size quantification, and analyses of inflammation and fibrosis, covering both acute and chronic stages of research.

Adapted for multi-cycle studies

The solution is flexible and customizable.

The durations of ischemia and reperfusion can be adjusted as needed, making it suitable for a wide range of mechanistic studies and drug‑efficacy evaluation projects.

Standardization of Data Delivery

One-stop efficient delivery

We have an in-house, end-to-end experimental platform, eliminating the need for external collaboration, thereby shortening project timelines and ensuring steady progress.

Modeling cycle

0h, 3h, 6h, 12h, 24h, 72h

1  Laboratory animals

Mice and rats of SPF grade

1  Positive drug

Commonly used drugs such as trimetazidine, enalapril, and nifedipine serve as positive control agents and can effectively ameliorate myocardial ischemia, mitigate cardiomyocyte injury, and protect cardiac function.

1  Application areas

This model is widely employed in the screening of cardiovascular and cerebrovascular drugs, as well as in pharmacodynamic and safety evaluations. It is also utilized to investigate the pathogenic mechanisms underlying myocardial injury, oxidative stress, inflammation, and fibrosis, and can support preclinical studies related to novel drug target validation, intervention strategy development, and Investigational New Drug (IND) submissions.

Experimental results

Animal model construction

Myocardial ischemia: thoracic compression–induced ligation of the left anterior descending coronary artery (LAD)

Myocardial ischemia–reperfusion: The squeezing method is used, with procedures broadly similar to those for establishing myocardial ischemia. The key difference is that, in the ischemia–reperfusion model, the LAD is ligated with a sliding knot; after a specified period of ischemia, the free ends of the suture are gently pulled to loosen the knot, thereby restoring blood flow through the LAD and ensuring normal perfusion of the myocardium.

 

 

Imaging examination

The figure shows the results of M‑mode echocardiography: in the control group, ventricular wall motion was coordinated and systolic function was normal; in the model group, ventricular wall motion was reduced and the rate of systolic thickening was decreased, indicating impaired cardiac function and successful model establishment.

 

 

TTC staining

Under routine TTC staining, the infarcted area in the model group appears white, while the non‑infarcted area appears red. From the ligation site toward the apex, the percentage of the white infarcted area gradually increases, and cardiac sections near the apex become almost entirely white.

 

 

Evans Blue + TTC double staining

The Vans Blue + TTC double-staining method is a combined technique that visualizes the model group as follows: non‑ischemic areas appear blue, infarcted areas are white, and the at‑risk zone remains unstained, retaining the native red color of myocardial tissue. This approach allows simultaneous assessment of cardiomyocyte integrity and metabolic activity, and is primarily used to evaluate the relative sizes of the at‑risk and infarcted zones in animal models of cardiac ischemia–reperfusion injury, thereby visualizing the extent of post‑injury damage and enabling localization and analysis of myocardial infarction regions.

 

 

H&E staining

In the control group, the tissue architecture was normal, with no obvious inflammatory cell infiltration. In the model group, blue collagen deposition was observed at the infarct site, indicating marked fibrosis.

 

 

Positive drug data

The role and mechanism of trimetazidine as a positive drug in the treatment of myocardial ischemia can be referenced in the following literature: Function and Mechanism of Trimetazidine in Myocardial Infarction-Induced Myocardial Energy Metabolism Disorder Through the SIRT1-AMPK Pathway.

This study investigated the effects and underlying mechanisms of trimetazidine, using it as a positive control, in myocardial energy metabolism disorders induced by myocardial infarction. The results demonstrated that trimetazidine exerts cardioprotective effects by modulating the SIRT1–AMPK signaling pathway. Employing a comprehensive array of assays—including HE staining of myocardial tissue, biochemical measurement of serum cardiac injury biomarkers, assessment of myocardial ATP levels, Western blot quantification of pathway‑related proteins, evaluation of oxidative stress markers, and TUNEL assay for apoptosis—data revealed that the drug effectively activates the expression of SIRT1 and AMPK proteins, restores dysregulated myocardial carbohydrate and lipid metabolism, attenuates myocardial inflammatory infiltration, myofiber necrosis, and interstitial edema, and reduces both oxidative stress levels and the rate of cardiomyocyte apoptosis. Consistent findings across multiple morphological, biochemical, and molecular parameters underscore the significant and robust therapeutic benefits of trimetazidine in mitigating myocardial ischemic injury, establishing it as a reliable positive control in models of myocardial ischemia.