CAJ | 학술논문

目的：通过分析颈动脉支架术患者血清中内皮型一氧化氮合酶（eNOS）的表达及血管内皮功能的改变，进一步探讨支架术后再狭窄的机制。方法将符合入组标准的患者根据是否有手术指征分为颈动脉支架组、颈动脉粥样硬化组。在入组前及术后1 h、1个月、6个月抽血采用ELISA测定血清eNOS，并测定血管内皮功能及颈动脉内膜中层厚度（IMT）。结果动脉粥样硬化组组内不同时间点血清eNos、IMT、血管舒张反应（FMD）比较差异无统计学意义（F＝16.156，13.009，11.785，P＞0.05）；颈动脉支架组在支架置入后血清eNOS表达水平明显下降，FMD下降、颈动脉内膜厚度增厚，两组比较差异有统计学意义（F＝104.521，176.501，167.116，P＜0.05）；阿托伐他汀治疗后血清eNOS表达水平上调，FMD上升、颈动脉内膜厚度下降并与剂量相关，差异有统计学意义（F＝123.328，207.442，206.721，P＜0.05）；颈动脉支架组与动脉粥样硬化组比较差异有统计学意义（F＝134.812，P＜0.05）。结论 eNOS 可以抑制颈动脉支架术后血管内膜的增生，减少再狭窄发生。
목적：통과분석경동맥지가술환자혈청중내피형일양화담합매（eNOS）적표체급혈관내피공능적개변，진일보탐토지가술후재협착적궤제。방법장부합입조표준적환자근거시부유수술지정분위경동맥지가조、경동맥죽양경화조。재입조전급술후1 h、1개월、6개월추혈채용ELISA측정혈청eNOS，병측정혈관내피공능급경동맥내막중층후도（IMT）。결과동맥죽양경화조조내불동시간점혈청eNos、IMT、혈관서장반응（FMD）비교차이무통계학의의（F＝16.156，13.009，11.785，P＞0.05）；경동맥지가조재지가치입후혈청eNOS표체수평명현하강，FMD하강、경동맥내막후도증후，량조비교차이유통계학의의（F＝104.521，176.501，167.116，P＜0.05）；아탁벌타정치료후혈청eNOS표체수평상조，FMD상승、경동맥내막후도하강병여제량상관，차이유통계학의의（F＝123.328，207.442，206.721，P＜0.05）；경동맥지가조여동맥죽양경화조비교차이유통계학의의（F＝134.812，P＜0.05）。결론 eNOS 가이억제경동맥지가술후혈관내막적증생，감소재협착발생。
Objective To analyze the eNOS expression and endothelial function after carotid artery stenting in patients, and explore the mechanism of stent restenosis. Methods According to the indications of carotid stents, patients were divided to carotid atherosclerosis group and carotid artery stenting group. To measure the eNOS,endothelial function and the carotid artery IMT, at the beginning, 1 hour,1 month and 6 months of post-operative. Results The eNOS, IMT, vasodilation(FMD) of the carotid atherosclerosis group had no significant difference at different time points (F=16.156, 13.009, 11.785, P>0.05);After stent implantation the expression level of eNOS was significantly decreased FMD decreased, carotid artery intima-media thickness in the carotid artery stenting group, there was significant difference(F=104.521, 176.501, 167.116, P<0.05);The expression of eNOS and FMD were increased, carotid artery intima-media were thickness by atorvastatin and dose related its, there was significant difference(F=123.328, 207.442, 206.721, P<0.05);There was significant difference between the carotid artery stenting group and atherosclerosis group(F=134.812, P<0.05). Conclusion Endothelial nitric oxide synthase can inhibit carotid artery stenting intimal hyperplasia, reduce stent restenosis.