Zvast Biotechnology
The Pig Myocardial Ischemia Model is a standardized SCI-recognized large-animal model in translational cardiovascular medicine, myocardial injury repair, and preclinical evaluation of novel therapeutics and biomaterials for ischemic heart disease. Thoracotomy is performed to expose coronary arteries, and controllable ligation of left anterior descending artery (LAD) is implemented to induce persistent insufficient blood supply to the anterior left ventricular wall, establishing a stable microenvironment of acute myocardial ischemia or myocardial infarction. This model recapitulates pathological progression of clinical coronary heart disease, acute myocardial infarction and ischemic heart failure. Porcine cardiac anatomy, coronary distribution, ventricular volume, myocardial wall thickness, heart rate, blood pressure, myocardial metabolism, temporal progression of cardiomyocyte apoptosis and fibrosis are highly homologous to human myocardium. Compared with rodents and canine models, pigs possess sparse coronary collateral circulation, resulting in clear demarcation of ischemic regions after ligation and superior reproducibility of ischemic injury. The model supports adjustable ischemic duration, compatible with distinct research protocols including ischemia/reperfusion (I/R) injury and permanent myocardial infarction. Dynamic monitoring of cardiac function, myocardial necrosis, ventricular remodeling and interstitial fibrosis can be realized. Multi-index longitudinal follow-up within individual animals yields low intra-group variation. Surgical procedure, ischemic target, monitoring protocol and specimen harvesting timeline can be quantitatively standardized, and experimental reproducibility meets publication criteria of high-impact SCI journals focusing on cardiovascular diseases, stem cells and biomaterials. This model is widely adopted for preclinical efficacy and biosafety evaluation of cardioprotective drugs, stem cell transplantation, cardiac patches, injectable hydrogels, gene delivery systems, pro-angiogenic agents and anti-ventricular remodeling strategies.
Persistent ST-segment elevation in leads corresponding to ischemic territory can be observed immediately after coronary ligation. Postoperative echocardiography reveals regional wall motion abnormality in anterior left ventricle. Clear pale infarct scar can be visualized via terminal TTC staining with stable infarct size and acceptable intra-group variation. No extensive non-target myocardial necrosis occurs, and no massive animal death induced by intraoperative lethal arrhythmia. Fulfillment of above criteria confirms successful establishment of myocardial ischemia model, enabling reliable discrimination of therapeutic effects on myocardial injury, cardiac function and ventricular remodeling among experimental groups.
Massive cardiomyocyte loss replaced by fibrous connective scar is observed in ischemic region of model group; prominent inflammatory infiltration exists in infarct border zone. Histomorphometric parameters: infarct percentage of left ventricle and collagen volume fraction (CVF) are significantly higher than sham group. Numerous TUNEL-positive apoptotic cardiomyocytes are detected in peri-infarct zone. No extensive non-specific surgical necrosis is observed on sections, indicating controllable surgical trauma and baseline operative interference.
A stable myocardial ischemia model is defined as persistent hypoxic injury in target myocardium after coronary blood flow occlusion, accompanied by cardiomyocyte necrosis, inflammatory activation, subsequent collagen deposition and ventricular remodeling with satisfactory reproducibility. Owing to sparse coronary collateral circulation in miniature pigs, ischemic territory after LAD ligation is controllable. This model faithfully recapitulates pathological progression of acute ischemia in clinical coronary artery disease, and enables objective evaluation of drugs, biomaterials and cell preparations in restricting myocardial necrosis, inhibiting fibrosis and improving cardiac function, serving as core academic evidence verifying model reliability in translational cardiovascular research.
The miniature pig myocardial ischemia model represents the mainstream large-animal model of ischemic heart disease in cardiovascular SCI publications. Cardiac size, coronary anatomy and myocardial metabolism are highly analogous to human heart, exhibiting superior translational value compared with rodent models. Sparse coronary collaterals yield clear ischemic boundary and highly reproducible infarct size. Continuous intraoperative ECG and invasive hemodynamic monitoring are feasible. Multiple intervention approaches including intramyocardial injection, epicardial cardiac patch implantation and injectable hydrogel delivery can be implemented. Multi-layer indicators including cardiac function, infarct size, fibrosis and angiogenesis can be evaluated simultaneously. Long-term follow-up supports observation of ventricular remodeling progression. Complete data chain facilitates manuscript acceptance by authoritative SCI journals in cardiovascular medicine and biomaterials. It ranks among the preferred large-animal models for preclinical research on acute myocardial infarction and ischemic heart failure.
The Pig Myocardial Ischemia Model is mainly applied to elucidate the complete pathological cascade including cardiomyocyte necrosis, inflammatory response, cell apoptosis, angiogenesis, collagen deposition and ventricular remodeling after acute myocardial ischemia. It evaluates in vivo efficacy and biocompatibility of cardioprotective drugs, mesenchymal stem cells, cardiac hydrogels, epicardial patches, gene therapy and sustained-release formulations in suppressing cardiomyocyte apoptosis, promoting angiogenesis, reducing scar formation, improving cardiac function and delaying heart failure progression. It explores regulatory strategies targeting ischemic microenvironment, anti-oxidative and anti-fibrotic signaling pathways. This model supports preclinical safety and efficacy verification of novel therapeutic strategies for acute myocardial infarction, acting as a core standardized large-animal model for translational researches in ischemic heart disease, myocardial regeneration and cardiovascular biomaterials.
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