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Updated: Jul 29, 2026

LAD-Ligation: A Murine Model of Myocardial Infarction
Published on: October 14, 2009
Preferential uptake of intravenously administered hyaluronidase (Hyalosidase) by damaged rat myocardium
Insights
This study shows that 125I-labelled hyaluronidase is preferentially taken up by damaged heart tissue in a rat model of myocardial infarction. This enzyme may be useful for targeting damaged areas in the heart.
Area of Science:
- Cardiology
- Biochemistry
- Pharmacology
Background:
- Myocardial infarction (MI) is a leading cause of death worldwide.
- Accurate diagnosis and targeted therapy for MI remain critical challenges.
Purpose of the Study:
- To establish a rat model of myocardial infarction.
- To investigate the biodistribution of 125I-labelled hyaluronidase in this model.
Main Methods:
- Myocardial infarction was induced in rats by left-anterior coronary artery ligation.
- Plasma levels of creatine kinase, aspartate aminotransferase, and lactate dehydrogenase were measured to confirm MI.
- 125I-labelled hyaluronidase was administered intravenously, and its uptake in damaged and normal myocardium was assessed.
Main Results:
- Successful induction of myocardial infarction was confirmed by elevated cardiac enzyme levels.
- Intravenous administration of 125I-labelled hyaluronidase resulted in significantly higher uptake in the damaged myocardium compared to normal heart tissue.
Conclusions:
- The established rat model reliably replicates key features of human myocardial infarction.
- 125I-labelled hyaluronidase demonstrates preferential accumulation in infarcted cardiac tissue, suggesting potential as a diagnostic or therapeutic agent.
Abstract:
The induction of myocardial infarction in rats by ligation of the left-anterior coronary artery was confirmed by measurement of increased plasma levels of creatine kinase, aspartate aminotransferase and lactate dehydrogenase. Using this model system it has been established that intravenous administration of 125I-labelled hyaluronidase to rats resulted in a preferential uptake of the enzyme by damaged myocardium as compared to normal heart tissue.
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