Conventional Method of Cardiac Ischemia/Reperfusion Injury in Mice.

Abstract

Myocardial ischemia-reperfusion injury (IRI) after myocardial ischemia, cardiac surgery, or circulatory arrest leads to adverse cardiovascular outcomes. Primarily, no blood flow to the heart causes an imbalance between oxygen demand and supply, namely, ischemia, resulting in damage or dysfunction of the cardiac tissue. Early restoration of blood flow has been established to be the treatment of choice to prevent further tissue injury. Indeed, the use of thrombolytic therapy or primary percutaneous coronary intervention is the most effective strategy for reducing the size of a myocardial infarct and improving the clinical outcome. Unfortunately, restoring blood flow to the ischemic myocardium, named reperfusion, can also contribute to injury. This phenomenon was therefore termed myocardial IRI. Subsequent studies in animal models of acute myocardial infarction suggest that myocardial IRI accounts for up to 50% of the final size of a myocardial infarct. Consequently, many researchers aim to understand the underlying molecular mechanism of myocardial IRI to find therapeutic strategies that ultimately reduce the final infarct size. Despite numerous therapeutic strategies identified in laboratories, no clinical medicine specifically targeting IRI has yet been approved. Therefore, more relevant research is needed to develop promising therapeutic agents. In this respect, we will introduce a solid and reproducible experimental protocol to induce myocardial IRI in mice and test potent drug transfer during this surgical procedure.