Objective To study the mechanism of restenosis following percutaneous transluminal coronary angioplasty(PTCA),and to replicate a dynamic model of cell proliferation and remoulding of vascular wall at different time points in rabbits after intimal injury.Methods The model of restenosis in common carotid artery was established by balloon injury in 70 rabbits.The indexes such as lumen area,thickness and area of intima and media,and cross sectional area bounded by the external elastic lamina(EELA) were respectively measured by computer image analysis technology at the 1st,3rd,5th, 7th,14th,28th and 35th day after the injury.Results Endothelial cells were denudated at the 1st day after injury.The proliferation of vascular smooth muscle cell(VSMC) was detected on the surface of lumen at 3 days after injury.At the 7th day after injury,the neointima was formed and continuously thicken.The thickness and area of the neointima as well as extracellular matrix were gradually increased after 14 days,and were maximal after 35 days.The thickness and area of media were also gradually increased during 3～14 days and decreased after 28 days.Compared with non-injured vessel,the medial area was obviously increased at the 14th day.The lumen area was decreased at the 5th～7th day after injury and was obviously less than that of non~injured vessel after 14 days.The EELA was gradually increased at the 1st～7th day after injury,and reached its maximum at the 14th day.The EELA was declined gradually after 28 days.Conclusion The progress of restenosis(RS) can be simulated through the model of restenosis in common carotid artery of rabbit established by balloon injury.The intimal proliferation and vascular remodeling are the leading pathogenesis of restenosis.

Objective To explore phenotypic modulation of vascular smooth muscle cells(VSMC) and change of p38 mitogen-activated protein kinase(MAPK) expression after intimal injury of rabbit carotid arteries. Methods The model of vascular restenosis established by balloon injury of rabbit carotid common arteries was used.HE staining,immunohistochemistry staining and Western blot were used to detect the change of proliferation cell nuclear antigen(PCNA),smooth muscle ?-actin(SM?-actin),p38 expression and morphology of sham-injured arteries and injured arteries at different time points.Results ⑴The proliferating VSMC was observed on the side of the medium lumen at 1 day and on the surface of vascular lumen at 3 days after injury.The neointima was formed and gradually being thicken at 5～7 days,and the thickening was accelerated at 14～35 days after injury.⑵PCNA was negative in the medium and endothelium of sham-injured arteries.Positive cell rate of PCNA was gradually increased at 1～14 days in the medium and at 5～14 days in the neointima after injury,with the maximum rate at 14 days.However,it declined gradually after 28 days.Positive cell rate of PCNA in the neointima was slightly higher than that in the medium.⑶SM?-actin was positive in the medium,negative in the endothelium of sham-injured arteries.Positive cell area of SM?-actin initially decreased at 1 day in the medium after injury with the minimum rate at 3 days,but it increased gradually after 5 days.Expression of SM?-actin in the neointima was slightly less than that in the medium.⑷p38 expression was very low or negative in the medium of sham-injured arteries.Expression of p38 was sustained and increased at 1～35 days after injury with the most remarkable elevation at 3～14 days.Expression of p38 in the neointima was higher than that in the medium.There was positive relationship between the p38 expression and PCNA expression in the vascular wall at different time points after injury.Elevation of p38 was earlier than decrease of SM?-actin.Conclusion There was a close relationship between the phenotypic modulation and proliferating ability of VSMC.P38 participated in signal transduction of phenotypic modulation of VSMC after intimal injury.