血管内膜

"The endothelial cells which line our arteries are an important site of action for the vascular protective effects of polyphenols," explains Corder.

"血管内皮细胞是连续被覆在全身血管内膜的一层细胞群，是具有保护血管作用的多酚在血管内活动的重要场所。"

"The endothelial cells which line our arteries are an important site of action for the ascular protectie effects of polyphenols," explains Corder.

"血管内皮细胞是连续被覆在全身血管内膜的一层细胞群，是具有保护血管作用的多酚在血管内活动的重要场所。"

The degradating and redistributing of ECM were migration of VSMC and vascular remodeling through inhibiting the production of PDGF-BB and the activation of MMPs so to prevent the vascular stenosis.⑤Orthotopic hybridism in situ: The expression of MMP-3 increased after operation, the tendency and intensity were parallel to the expression of NF-κB. Tongxinluo could decrease the expression of MMP-3 and NF-κB. The study showed that the producting and activating of MMP-3 were modulated by NF-κB. The inhibition to the producting and activating of MMp-3 of Tongxinluo was mediated by inhibiting the activating of NF-κB. Conclusion ①The rabbit vascular stenosis model could be established successfully by plain balloon damage, the operation process was easy, economical and practical.

①单纯球囊损伤可成功建立典型家兔血管狭窄模型，操作方法简单，经济实用；②以VSMC增殖、迁移为主的内膜增厚以及以ECM降解、合成与再分布所致的血管重构是导致受损血管狭窄的根本原因；③通心络能明显抑制VSMC的增殖、迁移和ECM降解、合成，阻止血管内膜增生和血管重构，防止受损血管狭窄；该作用可能与其减少和阻止PDGF-BB的产生和活性，以及抑制MMPs的表达和恢复MMPs/TIMPs平衡有关；④通心络能显著抑制球囊损伤后血管内膜增生和血管重构，可能与其保护血管内皮，改善内皮功能，增加血清NO含量有关；⑤通心络抑制内膜增生和血管重构，减轻受损血管狭窄，还可能是通过抑制NF-κB的活化途径而起作用的。

Inhibition of intimal hyperplasia or improvement of intima formation and vessel wall remodeling can effectively prevent restenosis.

抑制血管内膜过度增生或改善新生内膜形成以及血管重塑过程均可有效防止再狭窄。

GD can notedly decrease the expression of NF-κB and NF-κB mRNA in the abdominal aorta of AS rabbits damaged with sacculus proprius, and then may prevent the occurance of RS, which may he a part of the mechanism of preventive effect of GD.

冠心通络方减轻血管内膜增生、防止血管再狭窄的内在机制可能在于抑制NF-κB活性，进而抑制血管平滑肌细胞增殖、血管内膜增生。

"Anti-platelet drugs are often used to reduce intima thickening, for example, restenosis...after angioplasty. Perhaps a different method of inhibiting platelet activation would be to drink dealcoholized beer," Dr. Bassus says."Conversely, the acute consumption of alcohol beverages causes an increase of thrombin generation, suggesting a thrombotic risk in case of acute alcoholic intoxication."

抗血小板药物一般被用来降低血管内膜的肥厚症状，如该药物可预防血管修复手术后的血管狭窄现象，Bassus表示，也许抑制血小板活化的另一种方法就是投予去醇啤酒，然而，过度的酗酒反而会造成凝血酵素的增生，也就是说，急性酒精中毒通常会有缺血的风险。

Objective To study the relationship of endangium proliferation and the expression of metalloproteinases and tissue inhibitors of metalloproteinases after angioplasty of iliac artery in rabbits to investigate the probable mechanism of composite Danshen pill in prevention and treatment of restenosisMethods 30 white male rabbits of Japan （the average body weight was 25～30 kg）were randomly divided into 3 groups:normal control group,model group (intima destroyed by balloon and given hypercholesterol diet),CDP group (intima destroyed by balloon and given hypercholesterol diet plus drug CDP 150 mg/d),10 ones each groupResults The results of iliac artery angiogram and the analysis of pathology:there were lumens stenosis,thinner intima,smaller intima area,in CDP group compared with those in model group,and ratio of intima and tunica media thickness and area among each group (P＜001)Immunohistochemistry analysis:the MMP2,MMP9,TIMP1,TIMP2 in model group significantly increased than those in control group (P＜001)The CDP group had lower MMP2 and MMP9 expression,higher TIMP1 and TIMP2 expression,and increased MMP2/TIMP1,MMP9/TIMP2 than model group (P＜001)The thickening of vascular neointima and stenosis degree of vascular lumen were relevant to MMP2 and MMP9 (r=0896,P＜001)Conclusions MMP and TIMP play the very important role in the restenosis process of arteryCDP could inhibit the thickness of vascular neointima after balloon injury,the probable mechanism of which may be inhibiting collagen formation,smooth muscle immigration and decreasing hyperplasia of intima by interfering expression of MMPs and TIMPs

目的 研究兔髂动脉成形术后血管内膜增生和基质金属蛋白酶及其抑制物表达之间的关系，探讨复方丹参滴丸预防再狭窄的可能机制。方法健康成年二级雄性日本大耳白兔30只，平均体重25～30 kg。随机分为3组：正常对照组10只，模型组10只（球囊内膜剥脱加高胆固醇饮食），治疗组10只（球囊内膜剥脱加高胆固醇饮食以及复方丹参滴丸150 mg/d）。结果兔髂动脉造影、血管病理图像分析检测结果：①复方丹参滴丸组较模型组血管造影示管腔直径狭窄、内膜厚度减少、内膜面积减少、内膜厚度和中膜厚度比、面积比，各组之间有显著性差异(P＜001)。②免疫组化分析：模型组MMP2、MMP9、TIMP1、TIMP2表达均高于对照组（P＜001）；复方丹参滴丸组MMP2、MMP9的表达低于模型组，而TIMP1、TIMP2的表达高于模型组；TIMP1/MMP2、TIMP2/MMP9明显增加，差异有显著性（P＜001）。③内膜的增生以及管腔的狭窄程度与MMP2、MMP9有很好的相关性(r=0896，P＜001)。结论 MMP和TIMP在再狭窄形成中起重要作用；复方丹参滴丸能够明显抑制血管损伤后的内膜增生，可能的机制是通过影响金属蛋白酶MMP2、MMP9及其抑制物TIMP1、TIMP2的表达从而抑制胶原的生成、平滑肌的迁移、增生，而减少内膜的增生。

Methods: After transferred pcDNA3.1/hTM plasmid into rabbit artery by high-pressure injection, rabbit common iliac artery were cut and anastomosed again. At the 14 days and 28days after second operation, we checked inside diameter of anastomotic stoma and blood flow velocity by color Doppler. The treated artery were sliced and stained by Verhoeff. Local neointima formation and the ratio stenosis of intervascular were calculated by computer.

用注射式加压转染的方式对兔动脉壁转染pcDNA3.1/hTM质粒，再制造动脉损伤-阻滞模型，于术后14天、28天用彩色多普勒观察活体吻合口内径和血流流速；再做病理切片Verhoeff染色，观察血管内膜增生的程度、部位，计算血管内膜面积、中膜面积和血管狭窄率。

Intimal hyperplasia is one of the most critical problems in vascular surgery.

血管内膜增生是周围血管重建和再通手术后引起再狭窄的主要因素，是当前血管外科领域中最重要研究课题之一。

On the sixtieth postoperative day, the graft was harvested and the blood was taken from inferior cava venae. Histological changes were monitored by HE stain. The infiltration of CD4+ and CD8+ T lymphocytes and the expression ofα- smooth muscle actin were detected by immunohistochemistry.

术后60天取移植血管做病理组织学检查并利用计算机图象分析系统测量血管内膜厚度；免疫组织化学检测CD4+、CD8+T淋巴细胞的浸润及α-平滑肌肌动蛋白的表达；ELISA法检测血清中血管内皮生长因子的变化。

This one mode pays close attention to network credence foundation of the businessman very much.

这一模式非常关注商人的网络信用基础。

Cell morphology of bacterial ghost of Pasteurella multocida was observed by scanning electron microscopy and inactivation ratio was estimated by CFU analysi.

扫描电镜观察多杀性巴氏杆菌细菌幽灵和菌落形成单位评价遗传灭活率。