A novel survival model of cardioplegic arrest and cardiopulmonary bypass in rats: a methodology paper

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The model has several potential pitfalls. The endoaortic catheter requires exact and precise positioning close to the aortic valve. Ultrasonographic imaging is essential for positioning of the angioplasty catheter as well as assessing the cardioplegic arrest. When the catheter is not positioned optimally, incomplete arrest will be the result, and the balloon might even damage the brachiocephalic trunk (too high) or the left ventricle (too deep). If the injection of cardioplegia is executed too forcefully, dilatation of the left ventricle will occur. Measuring the pressure at the tip of the balloon catheter combined with the use of an infusion pump solves this issue. Use of the manufacturer™s inflation device prevents overinflation of the endoaortic balloon. After failed cardioplegic arrest on the first attempt, repeated small doses of cardioplegia will result in complete arrest. Although we did not measure potassium in these animals, earlier pilot experiments revealed that hyperkalemia does not occur with the dosing regimen used in this protocol. Immediate return to regular sinus rhythm at preoperative rates following deflation of the endoaortic balloon and restoration of preoperative hemodynamics present further indirect evidence that the cardioplegic regimen did not result in hyperkalemia.

As this work was entirely focused on developing the minimal invasive technique to accomplish CPB with cardioplegic arrest, we have not yet systematically investigated possible definite outcomes. However, study endpoints such as technical feasibility, effective cardioplegia, and survival were successfully demonstrated. The model described will not only facilitate further research to elucidate mechanisms of myocardial reperfusion injury following cardioplegic arrest and CPB but also to evaluate novel approaches to improved myocardial protection. Due to its minimal invasiveness and ease of recoverability, short- and long-term effects of constituents of cardioplegia, duration of cardioplegic arrest, CPB time, and potentially also direct gene transfer on myocardial function and histological outcomes can be assessed better than in isolated heart models. In addition, the model allows for the investigation of unique animal strains with varying susceptibility to myocardial injury depending on either their genetic background (consomic) or preexisting disease (e.g., diabetes, old age, hypertension).

Conclusion
This novel small animal CPB model with cardioplegic arrest allows for both the study of myocardial ischemia-reperfusion injury as well as the evaluation of new cardioprotective strategies. Major advantages of this model include its overall feasibility and cost effectiveness. In the field of myocardial protection, rodent models will remain an important avenue of research. Models such as the one described here will likely be utilized to not only assess longer-term functional outcomes but also characterize the enzymatic, genetic, and histologic response to myocardial injury and protective strategies.

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