| Since the late 1970s percutaneous transluminal coronary angioplasty (PTCA) has been widely applied in the therapy of coronary artery stenosis. Although the immediate success rate of PTCA has increased to more than 95%, long-term success was limited by significant restenosis of the arteryin 20-50% of patients within six months after the intervention. Proliferation of vascular smooth muscle cells, deposition of extracellular matrix, and infiltration of inflammatory cells with release of inflammatory mediators are implicated in the vascular restenosis seen after interventional procedures. Although experimental and clinical trials had been performed, it has been difficult to find the effective therapies against restenosis. In this study we used a balloon injury catheter to make the rat model of abdominal aortaendothelium injury. The prostaglandin E1(PGE1)was administered in the rat model via tail vein. The change of injured aortic endothelium, the plasma concentration of GMP-140. D-dimer. ET and the serum concentration of IL-1. IL-6. and TNF- a at different time points were studied to evaluate the effects of PGE1 preventing RS after balloon injury and its mechanisms.MethodsMale Wister rats were employed and randomly divided into five groups, namely, sham operation group, balloon injury model group and three PGEi dose (8. 24 . 72 gJcg-1) groups .Two procedures of experiments were performed. The rat vascular balloon injury model was made and the blood sample was collected in the first procedure of experiment. We inserted a special endothelial injury catheter with a balloon via rat left carotid artery to the bifurcation of common iliac artery injected 0.15ml NS to balloon, pulled balloon up and down for three times .to make abdominal aorta endothelial injury, then ligated left carotid artery. Whereas we only ligated left carotid artery in sham operation group. PGEi or NS was injected via tail vein one time per day for five days before operation in each group, the last injection was performed at 24th hour before operation. The underling experiments were performed in each group at the6th, 24th hour and the 10th ,21st day afrer operation :(1)we collected the blood sample from the rat heart, separated plasma or serum according the instruction, which was preserved in low temperature refrigerator for determination; ?The rats were sacrificed and abdominal aortic arteries were taken out , immersed in 4% formalin overnight, dried and put into the candle blocks. The second procedure of experiment included pathological investigation and analysis and determination of each kind of factors: CD the pathological specimen was sliced continuously, each slice was 4-5 u m thick, analyzed in IBAS computer system. (2) GMP-140,D-dimer concentration of the plasma was measured by ELISA double-layered antibody method, ET concentration of the plasma and IL- ,IL-6,TNF-a concentration of the serum was measured by radio-immunologic method.Results(1) Pathological observation: The vascular endothelial cell and internal elastic lamina were injured after balloon injury, medium layer and intima became thickened, and restenosis was occurred in model rats after three weeks. The proliferation of intima and medium areas were significantly decreased in PGEj ( 24,72 ) groups (P<0.01) .(2) the plasma levels ofGMP-140 and D-dimer in model group were significantly higher than that in sham group (P<0.01), PGE, ( 8,24,72 ug.kg-1) could significantly decrease the plasma levels of GMP-140 and D-dimer(PO.01 ) .(D the plasma level of ET increased at 6th hour after PTCA, reached maximum in 24th hours, then reduced gradually. PGE1 (24,72 P g.kg~') could significantly decrease the plasma levels of ET in 6th hour, 24th hour groups (P<0.01), but PGE, (8pgJcg"!) only could decrease the plasma level of ET in 24th hour groups (P<0.01 ) .(4) tfee serum level of TNF- a quickly reached maximum in 6th hours? the serum levels of IL-I P ,IL-6 reached maximum in 24th hours. PGEi( 8,24,72 p gJkg ) could significantly decrease the maximpaa serum levels of IL-I P...
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