2009Journal of Chinese MicrocirculationRequires access

The Changes of Histochemistry of Arterial Wall in Atherosclerosis Rats After Carotid Injury

En We

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Abstract

Objective To establish the common carotid catheter injury model in atherosclerosis rats and to study the pathogenesis of restenosis. Methods The balloon catheter injury was performed on the left common carotid artery of atherosclerosis rats with 2F balloon catheter. HE and Verhoeff staining were used to observe the dynamic change of neointimal and media hyperplasia at different time after injury. Immunohistochemistry was used to detect the proliferative cells and the change of SMα-actin expression. Results (1) At 7 days,the neointima formed and continuously thickened. At 3 months,the neointimal thickening reached a peak and vascular lumen was seriously narrow. Immunostain of SMα-actin was mostly positive in the neointimal and medial cells which show most of proliferative cells are smooth muscle cells. (2) The expression of SMα-actin was decreased from 2 days after balloon injury and then increased at 3 months. Conclusion Using of 2.0 balloon catheter can successfully establish the rat carotid injury model. Neointima hyperplasia occurs after balloon injury and results in lumen stenosis. VSMC phenotype transformation,proliferation,migration and extracellular matrix production play an important role in the processe of neointima hyperplasia.

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Objective To establish the common carotid catheter injury model in atherosclerosis rats and to study the pathogenesis of restenosis. Methods The balloon catheter injury was performed on the left common carotid artery of atherosclerosis rats with 2F balloon catheter. HE and Verhoeff staining were used to observe the dynamic change of neointimal and media hyperplasia at different time after injury. Immunohistochemistry was used to detect the proliferative cells and the change of SMα-actin expression. Results (1) At 7 days,the neointima formed and continuously thickened. At 3 months,the neointimal thickening reached a peak and vascular lumen was seriously narrow. Immunostain of SMα-actin was mostly positive in the neointimal and medial cells which show most of proliferative cells are smooth muscle cells. (2) The expression of SMα-actin was decreased from 2 days after balloon injury and then increased at 3 months. Conclusion Using of 2.0 balloon catheter can successfully establish the rat carotid injury model. Neointima hyperplasia occurs after balloon injury and results in lumen stenosis. VSMC phenotype transformation,proliferation,migration and extracellular matrix production play an important role in the processe of neointima hyperplasia.

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Available abstract

Objective To establish the common carotid catheter injury model in atherosclerosis rats and to study the pathogenesis of restenosis. Methods The balloon catheter injury was performed on the left common carotid artery of atherosclerosis rats with 2F balloon catheter. HE and Verhoeff staining were used to observe the dynamic change of neointimal and media hyperplasia at different time after injury. Immunohistochemistry was used to detect the proliferative cells and the change of SMα-actin expression. Results (1) At 7 days,the neointima formed and continuously thickened. At 3 months,the neointimal thickening reached a peak and vascular lumen was seriously narrow. Immunostain of SMα-actin was mostly positive in the neointimal and medial cells which show most of proliferative cells are smooth muscle cells. (2) The expression of SMα-actin was decreased from 2 days after balloon injury and then increased at 3 months. Conclusion Using of 2.0 balloon catheter can successfully establish the rat carotid injury model. Neointima hyperplasia occurs after balloon injury and results in lumen stenosis. VSMC phenotype transformation,proliferation,migration and extracellular matrix production play an important role in the processe of neointima hyperplasia.

Key concepts: Neointima, Restenosis, Lumen (anatomy), Medicine, Neointimal hyperplasia, Balloon catheter, Balloon, Angioplasty

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