Heart disease is the leading cause of death in the United States. Models to study myocardial injuries such as myocardial infarction are necessary to evaluate effective therapies towards such illnesses. This study aimed to validate the New Zealand White Rabbit as a model for myocardial infarction (MI). In this study, four rabbits were used to model ischemia and reperfusion injuries. In brief, each rabbit underwent general anesthesia using sodium pentobarbital at a rate of 20-40mg/kg/hour. Rabbits were intubated and mechanically ventilated using pure oxygen. While under anesthesia, the chest was opened, and cardiac ischemia was induced by occluding the middle region of the left anterior descending artery (LAD) for a period of one hour, followed by a period of reperfusion up to three hours. Serum chemistry and hematology was performed prior to and after ischemia/reperfusion injuries. Following reperfusion, hearts were excised and stained with 2,3,4-Triphenyltetrazolium (TTC) to evaluate myocardial infarction size.
Total infarct size was estimated to be between 5-25% on the middle section of the heart (corresponding with the area of occlusion). Total WBC count decreased from 7.64-8.95 x 103/μL to 2.23-3.65 x 103/μL after ischemia/reperfusion, but the percentage of neutrophils were increased from 9.7-17.0% to 27.5-66.5% of WBC after injury. Rabbits showed elevation in serum creatinine from 1.04-1.18mg/dL to 1.08-2.79mg/dL, and decreased levels of serum calcium from 13.9-15.0mg/dL to9.0-11.9mg/dL. Additionally, serum Cardiac Troponin I was elevated to 4.21-11.23ng/mL post ischemia/reperfusion, and was not detectable prior to injury. Taken together, this demonstrates this method of ischemia/reperfusion injury in rabbits does mimic MI, and Serum Cardiac Troponin I can function as an acute biomarker for MI.
Bouchard, G.F., Jones, M.R., Liu, J., Hiemstra, J.A., Stricker-Krongrad, A.