Myocardial Infarct and Ischemia Reperfusion Injury Models
Acute myocardial infarction (MI) is currently the leading cause of morbidity and mortality worldwide. MI occurs when myocardial ischemia exceeds a critical threshold and overwhelms myocardial cellular repair functions designed the maintain normal operating function and homeostasis. Risk factors for myocardial infarct include hyperlipidemia, diabetes, hypertension and heath factors (tobacco use, obesity etc).
The major cause of acute myocardial infarction (MI) is the complete or partial occlusion of one or more of the major coronary arteries resulting in inadequate blood flow to cardiac muscle tissue. A wide variety of experimental animal models are currently available for the study of MI and ischemic reperfusion (I/R) injury. In the rodent, occlusion of the left coronary artery is performed to mimic myocardial infarction in humans that results from occlusion of arteriosclerotic plaques of coronary arteries. Using this model, scientists can get a better understanding of the functional, structural and molecular changes associated with clinical ischemic heart disease as well as investigate the cardio-protection of potential drug therapies. Following the occlusion, the artery is opened directly to the heart making the occlusion-induced MI model particularly useful for therapies that work directly on the area of occlusion.
Histology for infarct
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Histology on four heart tissue samples from the vehicle treated group in the occlusion-induced ischemia reperfusion MI model in rats. Ischemia duration was 45 minutes and reperfusion was over 48 hours. Slides A-D: transverse section of the heart at 0.5x magnification. Slides E-H: 4x magnification of slides A-D showing the scarred myocardium.