Improvement and Assessment of modified New Zealand Rabbits Models of Myocardial Infarction_Chinese Journal of Clinical Thoracic and Cardiovascular Surgery

Authors：

HOUJiang-long ¹ , HANPeng-fei ² , XIEYu-ping ² , WANGHong-ge ² , GUOYing-kun ³ ,  WUZhong ¹

1. Department of Cardiovascular Surgery, West China Hospital, Sichuan University, Chengdu 610041, P. R. China;
2. Regenerative Medicine Research Center, West China Hospital, Sichuan University, Chengdu 610041, P. R. China;
3. Department of Radiology, West China Second University Hospital, Sichuan University, Chengdu 610041, P. R. China;

Corresponding author：

WUZhong, Email: wuzhong71@163.com

Keywords：

Myocardial infarction; Rabbit; Coronary artery; Animal model

DOI：

10.7507/1007-4848.20150093

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Objective To improve and assess the method of establishing myocardial infarction model in New Zealand rabbits. Methods A total of 60 New Zealand rabbits were randomly divided into two groups:the left anterior descending coronary artery was ligated in a LAD group (n=30); the left circumflex coronary artery was ligated in a LC group (n=30). Electrocardiogram (ECG), ultrasound cardiogram (UCG), hemodynamics and histology procedures were performed to detect the changes of cardiac structure and function after myocardial infarction induced by LAD and LC ligation. Results Success rate of the LC group was significantly higher than that in the LAD group (P < 0.01), but the survival rate in the LC group was slightly lower than the LAD group (P < 0.05); ECG within 24 h and 1 week after surgery showed that the average values of ST segment elevation in the LC group were significantly higher than that in the LAD group (P < 0.05); UCG and hemodynamics results showed cardiac function in the LAD group did not decrease significantly (P > 0.05). In contrast, cardiac function in the LC group were significantly decreased (P < 0.05). Histopathologic analysis showed that the area of myocardial infarction in the LC group was significantly larger than that in the LAD group (P < 0.01). Conclusion The myocardial infarction induced by the left circumflex coronary artery ligation is more consistent than that induced by the left anterior descending coronary artery ligation, suggesting that the former is a more appropriate experimental model for evaluations.

Citation： HOUJiang-long, HANPeng-fei, XIEYu-ping, WANGHong-ge, GUOYing-kun, WUZhong. Improvement and Assessment of modified New Zealand Rabbits Models of Myocardial Infarction. Chinese Journal of Clinical Thoracic and Cardiovascular Surgery, 2015, 22(4): 337-343. doi: 10.7507/1007-4848.20150093 Copy

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6.	Ellison GM, Torella D, Dellegrottaglie S, et al.Endogenous cardiac stem cell activation by insulin-like growth factor-1/hepatocyte growth factor intracoronary injection fosters survival and regeneration of the infarcted pig heart.J Am Coll Cardiol, 2011, 58(9):977-986.
7.	Teramoto N, Koshino K, Yokoyama I, et al.Experimental pig model of old myocardial infarction with long survival leading to chronic left ventricular dysfunction and remodeling as evaluated by PET.J Nucl Med, 2011, 52(5):761-768.
8.	Flore V, Claus P, Antoons G, et al.Microvolt T-wave alternans and beat-to-beat variability of repolarization during early postischemic remodeling in a pig heart.Heart Rhythm, 2011, 8(7):1050-1057.
9.	Noort WA, Feye D, Van Den Akker F, et al.Mesenchymal stromal cells to treat cardiovascular disease:strategies to improve survival and therapeutic results.Panminerva Med, 2010, 52(1):27-40.
10.	Zhao Q, Sun C, Xu X, et al.CD34+cell mobilization and upregulation of myocardial cytokines in a rabbit model of myocardial ischemia.Int J Cardiol, 2011, 152(1):18-23.
11.	Huang CH, Tsai SK, Chiang SC, et al.Brief pressure overload preconditions rabbit myocardium independent of adenosine receptor activation.Ann Thorac Surg, 2011, 92(5):1727-1732.
12.	Ripplinger CM, Lou Q, Li W, et al.Panoramic imaging reveals basic mechanisms of induction and termination of ventricular tachycardia in rabbit heart with chronic infarction:implications for low-voltage cardioversion.Heart Rhythm, 2009, 6(1):87-97.
13.	Feng Y, Xie Y, Wang H, et al.A modified rabbit model of reperfused myocardial infarction for cardiac MR imaging research.Int J Cardiovasc Imaging, 2009, 25(3):289-298.
14.	Hale SL, Kloner RA.Location as a determinant of myocardial infarction in rabbits.J Mol Cell Cardiol, 2000, 32(3):505-510.

1. Alsaid H, Bao W, Rambo MV, et al.Serial MRI characterization of the functional and morphological changes in mouse lung in response to cardiac remodeling following myocardial infarction.Magn Reson Med, 2012, 67(1):191-200.
2. Korf-Klingebiel M, Kempf T, Schluter KD, et al.Conditional transgenic expression of fibroblast growth factor 9 in the adult mouse heart reduces heart failure mortality after myocardial infarction.Circulation, 2011, 123(5):504-514.
3. Heusch G, Skyschally A, Schulz R.The in-situ pig heart with regional ischemia/reperfusion-ready for translation.J Mol Cell Cardiol, 2011, 50(6):951-963.
4. Wei YJ, Tang Y, Li J, et al.Cloning and expression pattern of dog SDF-1 and the implications of altered expression of SDF-1 in ischemic myocardium.Cytokine, 2007, 40(1):52-59.
5. 张洪宇, 庄建.不同停搏时间下, HTK液对幼兔未成熟心肌的保护作用.中国胸心血管外科临床杂志, 2015, 22(3):234-240.
6. Ellison GM, Torella D, Dellegrottaglie S, et al.Endogenous cardiac stem cell activation by insulin-like growth factor-1/hepatocyte growth factor intracoronary injection fosters survival and regeneration of the infarcted pig heart.J Am Coll Cardiol, 2011, 58(9):977-986.
7. Teramoto N, Koshino K, Yokoyama I, et al.Experimental pig model of old myocardial infarction with long survival leading to chronic left ventricular dysfunction and remodeling as evaluated by PET.J Nucl Med, 2011, 52(5):761-768.
8. Flore V, Claus P, Antoons G, et al.Microvolt T-wave alternans and beat-to-beat variability of repolarization during early postischemic remodeling in a pig heart.Heart Rhythm, 2011, 8(7):1050-1057.
9. Noort WA, Feye D, Van Den Akker F, et al.Mesenchymal stromal cells to treat cardiovascular disease:strategies to improve survival and therapeutic results.Panminerva Med, 2010, 52(1):27-40.
10. Zhao Q, Sun C, Xu X, et al.CD34+cell mobilization and upregulation of myocardial cytokines in a rabbit model of myocardial ischemia.Int J Cardiol, 2011, 152(1):18-23.
11. Huang CH, Tsai SK, Chiang SC, et al.Brief pressure overload preconditions rabbit myocardium independent of adenosine receptor activation.Ann Thorac Surg, 2011, 92(5):1727-1732.
12. Ripplinger CM, Lou Q, Li W, et al.Panoramic imaging reveals basic mechanisms of induction and termination of ventricular tachycardia in rabbit heart with chronic infarction:implications for low-voltage cardioversion.Heart Rhythm, 2009, 6(1):87-97.
13. Feng Y, Xie Y, Wang H, et al.A modified rabbit model of reperfused myocardial infarction for cardiac MR imaging research.Int J Cardiovasc Imaging, 2009, 25(3):289-298.
14. Hale SL, Kloner RA.Location as a determinant of myocardial infarction in rabbits.J Mol Cell Cardiol, 2000, 32(3):505-510.

Chinese Journal of Clinical Thoracic and Cardiovascular Surgery

Improvement and Assessment of modified New Zealand Rabbits Models of Myocardial Infarction

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