| PrefaceThe stenosis of coronary artery and peripheral artery is a kind of serious disease caused by arteriosclerosis. The disease threaten people's life and make them amputation and mutilation. At present, the autogenous vein graft's by - pass operation is still a chief therapeutic tool for the stenosis of coronary artery and peripheral artery. Untill now autogenous vein is the best translate materials. But these operations are often failure because of stenosis of vein grafts. The research of mechanism of restenosis and how to prevent and cure become the key point to improve therapeutic effectivness. That restenosis is mainly caused by intimal hyperplasia (IH) and sclerosis. Now it is proved that vessel smooth muscle cells ( VSMC ) transposition and hyperpro-liferation are the core pathologic change of IH. People have made great effort to prevent restenosis. They find many methods (including drugs and gene therapy) in experiments but unfortunately, they cant use into practice. The effective use of endovascular irradiation to prevent intimal proliferation in animal models of balloon arteral injury has already been demostrated in preclinical studies. Both y andp - emitter have been used in those research This study is to evaluate the effect of beta irradiation on the intimal proliferation and apoptosis in vein grafts.MethodsAutogenous vein graft model was established in 80 rats by transplanting internal branch of jugular vein to carotid artery by end to end anastomosis. After anesthetizing with 10% chloral hydrate (2ml/kg) , using mediam incision in cervical part, cutting skin, freeing jugular vein and common carotid artery, cutting jugular vein 0. 5cm, washing with heparin saline, using 11 - 0 no - injure suturing, end - to - end anastomosis jugular vein into common carotid artery. Two dose schedules were studied: (1) control group ( graft, nonirradiated ) ; ( 2) radiation group (20Gy). The veins were irradiated by P solution before anastomosis. The grafted veins were harvested at 3 day, 1 week, 2 week and 4 week respectively after the operation. IH (intimal hyper-plasia) , SMC (smooth muscle cell ) Proliferation, P53, bcl -2 and bax were observed with pathology and immunohistochemistry and analyzed by computer digitizing system. The presence of apoptotic VSMC was demonstrated by TUNEL method.ResultThere was a significant decrease in the intimal average thickness at 7 d, 14 d and 28 d (p <0.05) in the radiation group. Immunohis-tochemical analysis of PCNA indicated the decreased positive cell in the radiation compared with the control at 1 week and 2 week (p <0. 01). Apoptosis of VSMC in the radiation group was highter than the control group at 2 week (p <0. 01) . There is no significant difference between two groups in expression of P53, and there is significantincrease of bax /bcl - 2 in the radiation group at 2 week. ( p < 0. 05).DiscussionAfter years of study ,we have known the mechanism approximately. First vascular intima damages blood platelet aggregates and thrombosis. Second kinds of growth factors which regulated by some genes have been released. All above make IH and VSMC proliferated. HI and VSMC proliferation is a major cause of graft failure. People have made great effort to prevent restenosis.It was studied that irradiation may inhibit proliferation of VSMC and make the VSMC stay at the G0 - G1 stage. The synthesis of DNA in S stage will be decreased and then led the cells to apoptosis. Both the animal and preclinical experiments provide enough evidences to illuminate this phenomenon. PCNA(proliferating cell nuclear antigen) exits in every nucleus which in the cycle of proliferation. It is an objective target to reflect the level of proliferation. Our experiment proved that the percentage of positive cells of PCNA is declined in the irradiated group. Through this study local beta irradiation on vein graft may also inhibits IH and VSMC proliferation (p <0.05) and prompts the apoptosis of SMC.P53, bcl - 2 and bax are the important genes which regulated the apopto...
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