Establishment and Optimization of a Mouse Model of Myocardial Ischemia-Reperfusion Injury

Myocardial ischemia-reperfusion injury (MIRI) severely impairs cardiac prognosis after revascularization for acute myocardial infarction. Standardized mouse left anterior descending coronary artery (LAD) ligation models are widely used for MIRI research, yet conventional protocols rely on indwelling support tubes and secondary thoracotomy to restore reperfusion. Such procedures feature complicated operations, high risks of pneumothorax, severe thoracic trauma, and low batch modeling efficiency. To address these drawbacks, we established an optimized MIRI mouse model with a single thoracotomy and carbon-synthesis fishing line pull-out for reperfusion. Male C57BL/6 mice aged 6-8 weeks were divided into normal control (NC), traditional model (TM), and optimized model (OM) groups. Echocardiography, triphenyltetrazolium chloride (TTC) and hematoxylin-eosin (HE) staining, as well as serum inflammatory cytokines, lactate dehydrogenase (LDH), c-reactive protein (CRP), and myocardial injury marker cardiac troponin I (cTnI) levels were detected to compare modeling efficacy. Identical cardiac function, serum inflammatory cytokines, myocardial injury marker, infarct size, and myocardial pathological morphology changes were observed between TM and OM groups. The OM group displayed more homogeneous infarct regions and higher serum myocardial injury markers and cardiac function injury, indicating milder non-surgical trauma. Compared with the traditional method, this optimized procedure shortens surgical and anesthesia time, avoids fatal intraoperative pneumothorax, accelerates post-operative recovery, and improves animal survival. In conclusion, the optimized model produces equivalent MIRI lesions with higher safety, efficiency, and reproducibility. It serves as an ideal alternative to classic modeling approaches.