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.
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Chimenti, S., Carlo, E., Masson, S., Bai, A., Latini, R. (2004). Myocardial Infarction. In: Corti, A., Ghezzi, P. (eds) Tumor Necrosis Factor. Methods in Molecular Medicine™, vol 98. Humana Press. https://doi.org/10.1385/1-59259-771-8:217
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DOI: https://doi.org/10.1385/1-59259-771-8:217
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