Results Novel Method of MI or I / R Is More Efficient Than Classic Method With Shortened Recovery Time and Less Inflammation

Rationale: Coronary artery ligation to induce myocardial infarction (MI) in mice is typically performed by an invasive and time-consuming approach that requires ventilation and chest opening (classic method), often resulting in extensive tissue damage and high mortality. We developed a novel and rapid surgical method to induce MI that does not require ventilation. Objective: The purpose of this study was to develop and comprehensively describe this method and directly compare it to the classic method. Methods and Results: Male C57/B6 mice were grouped into 4 groups: new method MI (MI-N) or sham (S-N) and classic method MI (MI-C) or sham (S-C). In the new method, heart was manually exposed without intubation through a small incision and MI was induced. In the classic method, MI was induced through a ventilated thoracotomy. Similar groups were used in an ischemia/reperfusion injury model. This novel MI procedure is rapid, with an average procedure time of 1.22 0.05 minutes, whereas the classic method requires 23.2 0.6 minutes per procedure. Surgical mortality was 3% in MI-N and 15.9% in MI-C. The rate of arrhythmia was significantly lower in MI-N. The postsurgical levels of tumor necrosis factorand myeloperoxidase were lower in new method, indicating less inflammation. Overall, 28-day post-MI survival rate was 68% with MI-N and 48% with MI-C. Importantly, there was no difference in infarct size or post-MI cardiac function between the methods. Conclusions: This new rapid method of MI in mice represents a more efficient and less damaging model of myocardial ischemic injury compared with the classic method. (Circ Res. 2010;107:1445-1453.)

[1]  Yajing Wang,et al.  AMP-Activated Protein Kinase Deficiency Enhances Myocardial Ischemia/Reperfusion Injury but Has Minimal Effect on the Antioxidant/Antinitrative Protection of Adiponectin , 2009, Circulation.

[2]  W. Koch,et al.  Simultaneous Administration of Insulin‐Like Growth Factor‐1 and Darbepoetin Alfa Protects the Rat Myocardium Against Myocardial Infarction and Enhances Angiogenesis , 2008, Clinical and translational science.

[3]  David M. Harris,et al.  Targeted Inhibition of Cardiomyocyte Gi Signaling Enhances Susceptibility to Apoptotic Cell Death in Response to Ischemic Stress , 2008, Circulation.

[4]  W. Koch,et al.  Darbepoetin alfa, a long-acting erythropoietin analog, offers novel and delayed cardioprotection for the ischemic heart. , 2007, American journal of physiology. Heart and circulatory physiology.

[5]  M. Völkers,et al.  Cardiac S100A1 Protein Levels Determine Contractile Performance and Propensity Toward Heart Failure After Myocardial Infarction , 2006, Circulation.

[6]  E. Lakatta,et al.  Induction of myocardial infarcts of a predictable size and location by branch pattern probability-assisted coronary ligation in C57BL/6 mice. , 2004, American journal of physiology. Heart and circulatory physiology.

[7]  A. Dart,et al.  Serial echocardiographic assessment of left ventricular dimensions and function after myocardial infarction in mice. , 2000, Cardiovascular research.

[8]  J. J. Smith,et al.  Ventricular remodeling in a mouse model of myocardial infarction. , 1998, The American journal of physiology.

[9]  J. Fewell,et al.  A treadmill exercise regimen for identifying cardiovascular phenotypes in transgenic mice. , 1997, The American journal of physiology.