Myocardial infarction: animal models
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Published on: November 4, 2021
Stefano Chimenti1, Eleonora Carlo, Serge Masson
1Department of Cardiovascular Research, Mario Negri Institute for Pharmacological Research, Milan, Italy.
Insights
Myocardial ischemia/reperfusion in rodents models inflammation, aiding research into heart disease treatments. This approach helps study inflammatory mediators like tumor necrosis factor (TNF) and test anti-inflammatory drugs for myocardial infarction.
Area of Science:
- Cardiovascular Pathophysiology
- Inflammatory Response Mechanisms
- Experimental Myocardial Infarction Models
Background:
- Ischemic heart disease is a primary cause of heart failure and disability.
- Reperfusion, while essential, exacerbates myocardial injury through inflammation.
- Rodent models of myocardial ischemia/reperfusion are crucial for studying these processes.
Purpose of the Study:
- To highlight the utility of rodent models for investigating myocardial ischemia/reperfusion.
- To emphasize the role of inflammation in ischemia/reperfusion injury.
- To showcase the application of these models in evaluating therapeutic interventions.
Main Methods:
- Utilizing coronary artery occlusion and reperfusion in rodent models.
- Employing wild-type and transgenic animals, primarily mice.
- Assessing inflammatory mediators, including tumor necrosis factor (TNF).
Main Results:
- Ischemia/reperfusion models elicit a significant inflammatory response.
- These models facilitate the study of inflammation's role in acute injury and repair.
- The models are suitable for testing anti-inflammatory drugs.
Conclusions:
- Rodent models of myocardial ischemia/reperfusion are valuable for understanding cardiovascular pathologies.
- Inflammation is a key component of ischemia/reperfusion injury and subsequent repair.
- These models enable the assessment of therapeutic strategies for myocardial infarction.
Abstract:
Among the cardiovascular pathologies, ischemic heart disease is the leading cause of congestive heart failure as well as permanent premature disabilities. Reperfusion of a previously ischemic heart is a standard clinical procedure. Even if beneficial, reperfusion triggers an inflammatory response that contributes to the acute extension of ischemic injury and later participates in the reparative processes of the damaged myocardium. Occlusion of a major coronary artery in small rodents, followed or not followed by reperfusion, has proven to be a good model to assess the relevance of pathophysiological processes and drug effects in the setting of myocardial ischemia. Models involving reperfusion appear to be particularly suitable to study the inflammatory response, which is much more marked than with permanent ischemia. Ischemia/reperfusion of the myocardium in wild-type and transgenic animals (mostly mice) allows the possibility of testing the vast array of mediators that orchestrate the sequelae of inflammation, including tumor necrosis factor (TNF). Moreover, this model allows testing of the protective effects of anti-inflammatory drugs in experimental myocardial infarction.
