The swine heart is particularly suited to the study of human cardiovascular disease as its gross anatomy is very similar and its coronary microvasculature is nearly identical to that of humans – blood supply to the heart is right-side dominant and lacking in pre-existing collateral vessels. Physiologically, swine resting heart rates and left ventricular (LV) pressures are comparable to humans. Experimentally, swine offer advantages over smaller animal models of cardiovascular disease simply because of their larger size. For example, swine can tolerate multiple biopsies from the same tissues, intracoronary drug delivery, and implantation of microdialysis probes. [4,5] Swine have been used in the development and testing of intravascular stents, aneurysm surgery, valve replacement, cardiac transplant, and cardiac assist devices. [1] They have also served as important pre-clinical models for testing of new pharmacological agents and more recently stem cell therapy and gene therapy. Stem cells administered to swine post-myocardial infarction (MI) have been shown to decrease MI expansion and improve LV ejection fraction and gene therapy results using a swine model of heart failure (HF) have proved so effective that clinical trials have already begun. [4]
Swine also function as important models of MI, ischemia reperfusion (IR) injury, HF, and dilated cardiomyopathy (DCM). One of the main advantages of the use of swine as a model of cardiovascular disease is the ease with which MI can be produced in predictable sizes and locations analogous to MI in humans. Thus, swine are commonly used in pre-clinical studies investigating new strategies for limiting IR injury, infarct expansion, and LV remodeling. Post-MI, swine are positively affected by all of the cardioprotective strategies currently available for humans including hibernation and ischemic pre- and post-conditioning. Swine HF closely mimics that of humans in many respects as LV functions is depressed (i.e., myocyte contractility is impaired and ejection fraction is reduced) and the neurohormonal axis is activated. Additionally, DCM brought on by pacing-induced tachycardia in swine approximates the human DCM phenotype as it results in LV dilation, pump dysfunction, and neurohormonal changes similar to clinical observations. [4,5]
4. Dixon, J.A. and Spinale, F.G. (2009) Large animal models of heart failure: a critical link in the translation of basic science to clinical practice. Circ. Heart Fail. 2(3):262-271.
5. Heusch, G. et al. (2011) The in-situ pig heart with regional ischemia/reperfusion – ready for translation. J. Mol. Cell. Cardiol. [Epub ahead of print, Mar 5].
Swine also function as important models of MI, ischemia reperfusion (IR) injury, HF, and dilated cardiomyopathy (DCM). One of the main advantages of the use of swine as a model of cardiovascular disease is the ease with which MI can be produced in predictable sizes and locations analogous to MI in humans. Thus, swine are commonly used in pre-clinical studies investigating new strategies for limiting IR injury, infarct expansion, and LV remodeling. Post-MI, swine are positively affected by all of the cardioprotective strategies currently available for humans including hibernation and ischemic pre- and post-conditioning. Swine HF closely mimics that of humans in many respects as LV functions is depressed (i.e., myocyte contractility is impaired and ejection fraction is reduced) and the neurohormonal axis is activated. Additionally, DCM brought on by pacing-induced tachycardia in swine approximates the human DCM phenotype as it results in LV dilation, pump dysfunction, and neurohormonal changes similar to clinical observations. [4,5]
4. Dixon, J.A. and Spinale, F.G. (2009) Large animal models of heart failure: a critical link in the translation of basic science to clinical practice. Circ. Heart Fail. 2(3):262-271.
5. Heusch, G. et al. (2011) The in-situ pig heart with regional ischemia/reperfusion – ready for translation. J. Mol. Cell. Cardiol. [Epub ahead of print, Mar 5].
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