A piglet model of pulmonary vein stenosis_Chinese Journal of Clinical Thoracic and Cardiovascular Surgery

Authors：

ZHU Fang , WEN Chen , SHI Guocheng , ZHANG Qian , MU Hongwei , LIU Gang , SHI Bowen , YAN Yichen , ZHU Zhongqun ,  CHEN Huiwen

Department of Cardiothoracic Surgery, Shanghai Children’s Medical Center, Shanghai Jiaotong University School of Medicine, Shanghai, P.R.China;

Corresponding author：

CHEN Huiwen, Email: chenhuiwen@scmc.com.cn

Keywords：

Pulmonary vein stenosis; animal testing alternatives; pulmonary vein; pathology; myofibroblast

DOI：

10.7507/1007-4848.201812074

Video：

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Objective Pulmonary vein banding was used to establish a piglet model of pulmonary vein stenosis. We investigated the pathomorphological alterations of pulmonary veins in the model and compared it with the vascular tissue of recurrent stenosis after total anomalous pulmonary venous connection (TAPVC).Methods Ten pigs of 6 weeks old were selected and randomly divided into 2 groups: 5 in a sham operation group and 5 in a pulmonary vein banding group. The operation had two stages, in which thoracotomies through intercostal space were done respectively on both sides. Biocompatible materials were applied around the pulmonary veins in the experimental group. The same method was used in the sham group. But the pulmonary veins were not banded. Six weeks after the operation, the pulmonary veins of the animals were harvested for hematoxylin-eosin staining and immunofluorescence staining to observe the pathological alterations of pulmonary veins. The proliferative tissues of patients with recurrent stenosis after TAPVC repair were collected and observed by hematoxylin-eosin staining and immunofluorescence staining.Results Both the sham operation group and the pulmonary vein banding group survived. But the pulmonary vein banding group had obvious clinical manifestations of pulmonary venous stenosis. Compared with the sham group, the pulmonary vein banding group showed intimal hyperplasia, decreased expression of endothelial marker and increased expression of mesenchymal markers, and co-expression of endothelial and mesenchymal markers in intimal cells. Human pathology also showed intimal hyperplasia and co-expression of endothelial and mesenchymal markers in intimal cells.Conclusion The surgical pulmonary vein stenosis in piglets shows intimal hyperplasia and myofibroblasts, which was consistent with clinical pathology.

Citation： ZHU Fang, WEN Chen, SHI Guocheng, ZHANG Qian, MU Hongwei, LIU Gang, SHI Bowen, YAN Yichen, ZHU Zhongqun, CHEN Huiwen. A piglet model of pulmonary vein stenosis. Chinese Journal of Clinical Thoracic and Cardiovascular Surgery, 2019, 26(10): 1008-1013. doi: 10.7507/1007-4848.201812074 Copy

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3.	Kalfa D, Belli E, Bacha E, et al. Primary pulmonary vein stenosis: Outcomes, risk factors, and severity score in a multicentric study. Ann Thorac Surg, 2017, 104(1): 182-189.
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5.	Backes CH, Nealon E, Armstrong AK, et al. Pulmonary vein stenosis in infants: a systematic review, meta-analysis, and meta-regression. J Pediatr, 2018, 198: 36-45.
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7.	Devaney EJ, Chang AC, Ohye RG, et al. Management of congenital and acquired pulmonary vein stenosis. Ann Thorac Surg, 2006, 81(3): 992-995.
8.	Kalfa D, Belli E, Bacha E, et al. Outcomes and prognostic factors for postsurgical pulmonary vein stenosis in the current era. J Thorac Cardiovasc Surg, 2018, 156(1): 278-286.
9.	LaBourene JI, Coles JG, Johnson DJ, et al. Alterations in elastin and collagen related to the mechanism of progressive pulmonary venous obstruction in a piglet model. A hemodynamic, ultrastructural, and biochemical study. Circ Res, 1990, 66(2): 438-456.
10.	Kato H, Fu YY, Zhu J, et al. Pulmonary vein stenosis and the pathophysiology of "upstream" pulmonary veins. J Thorac Cardiovasc Surg, 2014, 148(1): 245-53.
11.	Riedlinger WF, Juraszek AL, Jenkins KJ, et al. Pulmonary vein stenosis: expression of receptor tyrosine kinases by lesional cells. Cardiovasc Pathol, 2006, 15(2): 91-99.
12.	Li S, Li H, Mingyan E, Yu B. Expression of TGFbeta1 in pulmonary vein stenosis after radiofrequency ablation in chronic atrial fibrillation of dogs. Mol Biol Rep, 2009, 36(2): 221-225.
13.	Moonen JR, Lee ES, Schmidt M, et al. Endothelial-to-mesenchymal transition contributes to fibro-proliferative vascular disease and is modulated by fluid shear stress. Cardiovasc Res, 2015, 108(3): 377-86.
14.	Vanderlaan R, Fu Y, Rai N, et al. Abstract 20169: The role of pathological strain on pulmonary vein endothelial cells. Circulation, 2017, 136(suppl_1): A20169-A.
15.	Krenning G, Barauna VG, Krieger JE, et al. Endothelial plasticity: shifting phenotypes through force feedback. Stem Cells Int, 2016, 2016: 9762959.

1. Seale AN, Uemura H, Webber SA, et al. Total anomalous pulmonary venous connection: morphology and outcome from an international population-based study. Circulation, 2010, 122(25): 2718-2726.
2. Shi G, Zhu Z, Chen J, et al. Total anomalous pulmonary venous connection: the current management strategies in a pediatric cohort of 768 patients. Circulation, 2017, 135(1): 48-58.
3. Kalfa D, Belli E, Bacha E, et al. Primary pulmonary vein stenosis: Outcomes, risk factors, and severity score in a multicentric study. Ann Thorac Surg, 2017, 104(1): 182-189.
4. Karamlou T, Gurofsky R, Al Sukhni E, et al. Factors associated with mortality and reoperation in 377 children with total anomalous pulmonary venous connection. Circulation, 2007, 115(12): 1591-1598.
5. Backes CH, Nealon E, Armstrong AK, et al. Pulmonary vein stenosis in infants: a systematic review, meta-analysis, and meta-regression. J Pediatr, 2018, 198: 36-45.
6. Packer DL, Keelan P, Munger TM, et al. Clinical presentation, investigation, and management of pulmonary vein stenosis complicating ablation for atrial fibrillation. Circulation, 2005, 111(5): 546-554.
7. Devaney EJ, Chang AC, Ohye RG, et al. Management of congenital and acquired pulmonary vein stenosis. Ann Thorac Surg, 2006, 81(3): 992-995.
8. Kalfa D, Belli E, Bacha E, et al. Outcomes and prognostic factors for postsurgical pulmonary vein stenosis in the current era. J Thorac Cardiovasc Surg, 2018, 156(1): 278-286.
9. LaBourene JI, Coles JG, Johnson DJ, et al. Alterations in elastin and collagen related to the mechanism of progressive pulmonary venous obstruction in a piglet model. A hemodynamic, ultrastructural, and biochemical study. Circ Res, 1990, 66(2): 438-456.
10. Kato H, Fu YY, Zhu J, et al. Pulmonary vein stenosis and the pathophysiology of "upstream" pulmonary veins. J Thorac Cardiovasc Surg, 2014, 148(1): 245-53.
11. Riedlinger WF, Juraszek AL, Jenkins KJ, et al. Pulmonary vein stenosis: expression of receptor tyrosine kinases by lesional cells. Cardiovasc Pathol, 2006, 15(2): 91-99.
12. Li S, Li H, Mingyan E, Yu B. Expression of TGFbeta1 in pulmonary vein stenosis after radiofrequency ablation in chronic atrial fibrillation of dogs. Mol Biol Rep, 2009, 36(2): 221-225.
13. Moonen JR, Lee ES, Schmidt M, et al. Endothelial-to-mesenchymal transition contributes to fibro-proliferative vascular disease and is modulated by fluid shear stress. Cardiovasc Res, 2015, 108(3): 377-86.
14. Vanderlaan R, Fu Y, Rai N, et al. Abstract 20169: The role of pathological strain on pulmonary vein endothelial cells. Circulation, 2017, 136(suppl_1): A20169-A.
15. Krenning G, Barauna VG, Krieger JE, et al. Endothelial plasticity: shifting phenotypes through force feedback. Stem Cells Int, 2016, 2016: 9762959.

Chinese Journal of Clinical Thoracic and Cardiovascular Surgery

A piglet model of pulmonary vein stenosis

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