IN VIVO ENDOTHELIAL INJURY AND DEPENDENT VASOMOTION

内皮依赖性血管松弛功能受损 (EDVR)在冠状动脉中的活体表达可能与 部分由冠状动脉危险因素引起的内皮损伤量 因子与猪和患者的动脉粥样硬化 通过降低风险因素而减少。动脉中的血管收缩可以 减少血流量，增加动脉壁剪切力 增加受损动脉中的血小板沉积，并可能 沉淀动脉粥样硬化斑块破裂。内皮细胞 能代谢和减少血管壁内扩散 血管内收缩物质(血小板制品和 儿茶酚胺)，防止血小板活化和随后 释放血小板血管收缩物质，促进 前列环素和前列环素的产生和释放引起的血管扩张 血管内皮源性松弛因子(EDRF)。 在猪身上，我们将检验这样的假设：节段性冠状动脉 EDVR的动脉损伤(通过定量测量 血管造影术)到分级注射乙酰胆碱(一种EDRF- 释放剂)与血管内皮损伤程度相关 (以111In标记的自体血小板的程度来定量 “1998年书面供词(第(血小板/立方厘米)以及表面积的百分比 伊文思蓝染色区域)(A)轻度球囊扩张， (b，c)内皮样细胞再生后4天和8天 球囊损伤后，(D)喂饲2%胆固醇4mo。 (E)4个月后内皮愈合或再生 停喂胆固醇，(F)由4%的8mo诱导 胆固醇喂养，在其近端、上覆和远端位置 动脉粥样硬化病变超过50%，以及(G)4个月后 停止饲喂4%的胆固醇。 EDVR冠脉节段性损害患者的临床研究 (通过定量冠状动脉造影术测量)到分级 注射乙酰胆碱可以作为一种探针来研究 内皮损伤的严重程度(以及损伤的程度和时机 愈合或再生)病变最小的冠状动脉 (A)降低升高的甘油三酯和 胆固醇，(B)降低升高的胆固醇，和(C) 戒烟。冠状动脉节段性损害 EDVR也可以作为测量时间和程度的探头 球囊近端和远端的内皮愈合 血管成形术(血管内皮损伤但不顺利 肌肉细胞坏死)，在术后出现症状的动脉 心肌梗死或不稳定心绞痛，并确定 降低冠状动脉危险因素的水平是最佳的 内皮细胞的愈合。

The impairment of endothelial-dependent vascular relaxation (EDVR) in vivo in coronary arteries is probably related to the amount of endothelial injury induced in part by coronary risk factors and atherosclerosis in pigs and patients and may be reduced by risk factor reduction. Vasoconstriction in arteries can reduce blood flow, increase arterial wall-shear forces which increases platelet deposition in injured arteries, and may precipitate rupture of atherosclerotic plaques. The endothelium can metabolize and reduce the intramural diffusion of intraluminal vasoconstrictive substances (platelet products and catecholamines), prevent platelet activation and subsequent release of platelet vasoconstrictive substances, and promote vasodilation via the production and release of prostacyclin and endothelial-derived relaxing factor (EDRF). In the pig, we will test the hypothesis that the segmental coronary arterial impairment of EDVR (measured by quantitative angiography) to graded infusions of acetycholine (an EDRF- releasing agent) correlates with the extent of endothelial injury (quantitated by the degree of 111 In-labeled autologous platelet deposition (no. of platelets/cubic cm.) and the percent of surface area stained by Evans blue) (a) induced by mild balloon dilatation, (b, c) following regrowth of endothelial-like cells 4 and 8 days after balloon injury, (d) induced by 4 mo of 2% cholesterol feeding (e) following healing or regrowth of endothelium after 4 mo withdrawal of cholesterol feeding, (f) induced by 8 mo of 4% cholesterol feeding, in locations proximal, overlying, and distal to a greater than 50% atherosclerotic lesion, and (g) 4 mo after withdrawal from 4% cholesterol feeding. In patients segmental coronary arterial impairment of EDVR (measured by quantitative coronary angiography) to graded infusions of acetylcholine can be a probe to investigate the severity of endothelial injury (and the extent and timing of healing or regrowth) in minimally diseased coronary arteries before and after (a) reduction of elevated triglycerides and cholesterol, (b) reduction of elevated cholesterol, and (c) cessation of smoking. Segmental coronary arterial impairment of EDVR can also be a probe for measuring the timing and degree of endothelial healing just proximal and distal to the site of balloon angioplasty (where there is endothelial damage but no smooth muscle cell necrosis), in the symptom-producing artery after myocardial infarction or unstable angina, and for determining the level of coronary risk factor reduction necessary for optimal healing of the endothelium.