Abstract: Objective By means of the rat abdominal aortic allograft model,the purpose of this study is further to consider the vascular smooth muscle cells(VSMC)proliferating regulation in the course of allograft ateriosclerosis(AA)formation.Methods Inbred male Wistar rats served as donors and SD rats as recipients weighed 120~350g.There are three groups.A group:(acute rejection group),90 rats were killed postoperatively in 2,4 and 8 weeks.B group:(chronic rejection group),72 rats were killed in 4,8 and 12 weeks after operation.C group:(native control group) The rat abdominal aortic allograft model was used.Paraffin sections were stained with hematoxylin and eosin(HE),Masson and immuno histochemistry.HE staining was used to observe rejective degree in vessels;masson trichrome coloration was used to judge arteriosclerostic extent;and immunohistochemistry staining,to look into the number of A-actin positive expression in VSMC,and those cells expressing degree in cdk1/cyclinB1,cdk2/cyclin E,cdk4/cyclinD1.Results The most obvious lesion in A group was the intense interstitial adventitial infiltration by lymphocytes and mononuclear cells in a large ring around the vessels.At beginning,the inflammatory infiltration were mainly located in the outline of middle and adventitial membrane.Following time and course progressing,the number of A-actin positive cells in adventitia were increasing significantly.Those A-actin positive cells and vasa vasorum expressed PCNA,cdk's/cyclins remarkably,and all of endogenous regulatory proteins expressine degree were more higher followed by AA progression.The arteriosclerosis in chronic rejective group progressed slowly than A group,and intimal proliferation were equal to advertitia;VSMC in intimal and advertitia were all expressed cdk's/cyclins.In A and B groups,vasa vaso rumearly expressed A-actin,PCNA,cdk's and cyclins.Following inflammatory infiltration accelerately,they expressed more early and obviously.If vasa vasorum proliferated more fast and earlier,their caliber would be stenostic and occluded.Conclusion The result suggests that both acute and chronic rejection can cause AA.The former happened fast,the mainly pathologic changes were great deal of VSMC proliferation,inflammatory infiltration and fibrosclerosis in adventitia,and Proliferating VSMC expressed cdk1/cyclinB1,cdk2/cyclinE and cdk4/cyclinD1 greatly.The latter was mainly manifested by apparently intimal and adventitial VSMC proliferation,which were controlled by cdk's and cyclins.