Percutaneous transluminal coronary angioplasty (PICA) and stent implantation are the breakthrough of therapy of coronary artery disease in past two decades, but restenosis after the procedure is still the main problem affecting the outcoming. A lot of methods including drug, gene therapy, intracoronary radiation therapy, coated stent, failed to be the solution. Recently we tried to use magnetics to treat the problem and a sigle-center, small sample clinical trail showed that we may find the key.Every intervention aimed at increasing lumen size inevitably leads to damage of the vessel wall. The subsequent healing response, necessary to pacify the inflicted wound, triggers the growth of a neointimal thickening. Excessive growth of the neointimal thickening is only one of the contributors to restenosis after PTCA, but is likely the sole responsible factor when dealing with in-stent restenosis. PTCA mechanically damages the endothelial cells and induces endothelial dysfunction. Endothelial damages may be the trigger of in-stent hyperplasia. A functional endothelial lining is important in controlling the growth of the underlying vascular tissue, and enhancing the endothelial growth can inhibit neointimal growth. Therefore, the present study investigate the role of static magnetic field in endothelial proliferation, migrating, apoptosis and compare the common stent and magnetic stent with respect to the restenosis.-7-MethodsPART 1: In this part we investigated the effect of static magnetic field on the proliferation of human umbilical vascular endothelial cell and rabbit aorta endothelial cells; studied the influence of weak static magnetic field in inducing VEGF expressing by western blot method; observed the role of genistein and L-NAME in magnetic field changing the growth of human umbilical vascular endothelial cell and rabbit aorta endothelial cells; investigated the effect of weak static field on paraendocrine of endothelium and the influence of it to the proliferation of vascular smooth muscle cells; at last we measured the influences of static magnetic field to endothelial migration by a scratch injury model.PART n: this part is to produce more evidence to support the part I . In thispart firstly we measured the intracellular Ca+ concentration of endothelium, which pretreated with magnetics of 0.5Gs, IGs, lOGs for 30 min, with the fluoresent Ca+ indicator Fluo-3 and laser scanning confocal microscopy. Secondly with patch clamp technique, we comparatively measured Ca+ currents of endothelium, which pretreated with magnetics of O.SGs, IGs, lOGs for 30 min, through non-selective cation channel. The aim of this part is to investigate the signal transduction of how magnetics influenced the proliferation of endothelium.PART ffi in this part we compared the effect of different magnetics inintensity on the viability of endothelium. With transmission electric microscopy we observed the changes of endothelial utra-microstructure pretreated by different static magnetic field; by flow ctometry and TUNEL and transmission electric microscopy we measure the apoptosis rate of endothelium exposing in different static magnetics.PART IV: This part is relatively independent of the above three parts. In thispart we investigated the effects of static magnetic field on endothelium with respect to inflammation. We measured the adhesion of monocytes to endothelium treated by TNF a . In the mean time VCAM-1 expression was observed by flow cytometry and ELSIA.-8-PART V: This part is the destine of our study. In this part we compared theeffects of magnetic stent and common stent in neointimal hyperplasia and endothelial regeneration in porcine coronary model.Results and Conclusions1. The effect of static magnetic field on growth of human umbilical vascular vein endothelial cells and rabbit aorta endothelium is dependent in the magnetic intensity. O.SGs magnetics can accelerate the proliferation of endothelium; IGs magnetics have no effects on the growth of endothelium. wherease, magne