Burchenal J E, Keaney J F, Curran-Celentano J, Gaziano J M, Vita J A
Evans Department of Medicine, Whitaker Cardiovascular Institute, Boston University School of Medicine, MA, USA.
Atherosclerosis. 1996 Jun;123(1-2):157-67. doi: 10.1016/0021-9150(96)05801-7.
The success of percutaneous transluminal coronary angioplasty is limited by restenosis in 30-50% of cases. Cellular production of reactive oxygen species at the site of injury has been implicated as a contributing factor in the process of restenosis. beta-Carotene is a lipid-soluble antioxidant whose effects on this process have not been previously investigated. We attempted to elucidate whether beta-carotene treatment was capable of reducing restenosis. Femoral artery stenoses were produced by nitrogen-desiccation in rabbits fed a high-cholesterol diet. The animals were randomized to receive either a parenteral bolus of beta-carotene immediately prior to angioplasty, followed by 5 days of subcutaneous treatment (Acute Treatment); 5 days of subcutaneous pretreatment with beta-carotene followed by a parenteral bolus immediately prior to angioplasty and then another 5 days of subcutaneous treatment (Pretreatment); or vehicle only (Control). Angiography was performed immediately before and after angioplasty, and 28 days after angioplasty. The animals were then sacrificed, and the femoral arteries were harvested for histopathology. By quantitative angiography, the late loss of luminal diameter between angioplasty and final angiography was not significantly different between the acute treatment group, the pretreatment group and the control group. By histopathology, the area of intimal hyperplasia and the percent cross-sectional area stenosis were also not significantly different. The late loss in luminal diameter after angioplasty correlated significantly with the acute gain in luminal diameter produced by angioplasty. The amount of intimal hyperplasia correlated significantly with the arterial injury score assessed by histopathology. In summary, in this animal model of restenosis, parenteral beta-carotene failed to significantly reduce the amount of either intimal hyperplasia or late loss in luminal diameter after angioplasty.
经皮腔内冠状动脉成形术的成功率受到再狭窄的限制，30%-50%的病例会出现再狭窄。损伤部位细胞产生活性氧被认为是再狭窄过程中的一个促成因素。β-胡萝卜素是一种脂溶性抗氧化剂，其对这一过程的影响此前尚未得到研究。我们试图阐明β-胡萝卜素治疗是否能够减少再狭窄。通过对喂食高胆固醇饮食的兔子进行氮气干燥来制造股动脉狭窄。将动物随机分为三组，一组在血管成形术之前立即接受一次β-胡萝卜素静脉推注，随后进行5天的皮下治疗（急性治疗组）；一组先进行5天的β-胡萝卜素皮下预处理，在血管成形术之前立即接受一次静脉推注，然后再进行5天的皮下治疗（预处理组）；另一组只给予赋形剂（对照组）。在血管成形术前后以及血管成形术后28天进行血管造影。然后处死动物，采集股动脉进行组织病理学检查。通过定量血管造影，急性治疗组、预处理组和对照组在血管成形术和最终血管造影之间管腔直径的后期丢失没有显著差异。通过组织病理学检查，内膜增生面积和横截面积狭窄百分比也没有显著差异。血管成形术后管腔直径的后期丢失与血管成形术产生的管腔直径急性增加显著相关。内膜增生量与通过组织病理学评估的动脉损伤评分显著相关。总之，在这个再狭窄动物模型中，静脉注射β-胡萝卜素未能显著减少血管成形术后内膜增生量或管腔直径的后期丢失。
