Related Experiment Video
Updated: Mar 25, 2026
Myocardial Infarction and Functional Outcome Assessment in Pigs
Published on: April 25, 2014
Pathological observation of acute myocardial infarction in Chinese miniswine
Chuang Wang1, Shao-Xin Wang1, Ping-Shuan Dong1
1Department of Cardiology, The First Affiliated Hospital, Henan University of Science and Technology Jinghua Road No. 24, Luoyang 471003, China.
Abstract:
The acute myocardial infarction (AMI) model in Chinese miniswine was built by percutaneous coronary artery occlusion. Pathological observation of AMI was performed, and the expression of tumor necrosis factor alpha (TNF-α) in the infarct sites was detected at different days after modeling in Chinese miniswine. The experimental findings may be used as the basis for blood flow reconstruction and intervention after AMI. Seven experimental Chinese miniswine were subjected to general anesthesia and Seldinger right femoral artery puncture. After coronary angiography, the gelfoam was injected via the microtube to occlude the obtuse marginal branch (OM branch). At 1 d, 3 d, 5 d, 7 d, 10 d, 14 d and 17 d after modeling, hetatoxylin-eosin (HE) staining was performed to observe the pathological changes and to detect the expression of TNF-α in the myocardial tissues. Cytoplasmic acidophilia of the necrotic myocardial tissues at 1 d after modeling was enhanced, and cytoplasmic granules were formed; at 3 d, the margins of the necrotic myocardial tissues were infiltrated by a large number of inflammatory cells; at 5 d, the nuclei of the necrotic myocardial cells were fragmented; at 7 d, extensive granulation tissues were formed at the margin of the necrotic myocardial tissues; at 10 d, part of the granulation tissues were replaced by fibrous scar tissues; at 14-17 d, all granulation tissues were replaced by fibrous scar tissues. Immunohistochemical detection indicated that no TNF-α expression in normal myocardial tissues. The TNF-α expression was first detected at 3 d in the necrotic myocardial tissues and then increased at 5 d and 7 d. After reaching the peak at 10 d, the expression began to decrease at 14 d and the decrease continued at 17 d. Coronary angiography showed the disappearance of blood flow at the distal end of OM branch occluded by gelfoam, indicating that AMI model was constructed successfully. The repair of the infarcted myocardium began at 10-17 d after modeling with safe blood flow reconstruction. TNF-α expression in the infarcted myocardium was the highest at 10 d, which can be explained by inflammation and repair of the infarcted myocardium.
Insights
This study successfully created an acute myocardial infarction (AMI) model in Chinese miniswine. Tumor necrosis factor alpha (TNF-α) expression peaked at 10 days, correlating with myocardial inflammation and repair processes.
Area of Science:
- Cardiovascular Research
- Pathology
- Biomedical Engineering
Background:
- Acute myocardial infarction (AMI) is a leading cause of mortality worldwide.
- Understanding the temporal dynamics of inflammation and tissue repair post-AMI is crucial for developing effective treatments.
- Chinese miniswine offer a relevant preclinical model for studying human cardiovascular diseases.
Purpose of the Study:
- To establish a reliable percutaneous coronary artery occlusion model of AMI in Chinese miniswine.
- To characterize the pathological changes and temporal expression patterns of tumor necrosis factor alpha (TNF-α) in the infarcted myocardium.
- To provide a basis for future studies on blood flow reconstruction and therapeutic interventions following AMI.
Main Methods:
- AMI was induced in Chinese miniswine by percutaneous occlusion of the obtuse marginal (OM) branch using gelfoam injection.
- Pathological changes were assessed using hematoxylin-eosin (HE) staining at various time points post-modeling (1-17 days).
- Tumor necrosis factor alpha (TNF-α) expression was detected via immunohistochemistry in myocardial tissues.
Main Results:
- Successful induction of AMI was confirmed by coronary angiography showing occluded OM branch and absent blood flow.
- Histopathological analysis revealed progressive myocardial necrosis, inflammatory cell infiltration, granulation tissue formation, and eventual scar tissue replacement.
- TNF-α expression was absent in normal myocardium, first detected at 3 days post-AMI, peaking at 10 days, and declining by 14-17 days, coinciding with peak inflammation and early repair stages.
Conclusions:
- The established Chinese miniswine AMI model accurately reflects pathological progression and inflammatory responses.
- Temporal TNF-α expression correlates with the inflammatory and reparative phases of myocardial infarction.
- This model serves as a valuable platform for investigating therapeutic strategies aimed at mitigating AMI damage and promoting myocardial recovery.
