Stevens S L, Hilgarth K, Ryan U S, Trachtenberg J, Choi E, Callow A D
Washington University School of Medicine, Department of Surgery, St. Louis, Missouri 63110.
Ann Vasc Surg. 1992 Jan;6(1):55-61. doi: 10.1007/BF02000669.
In an attempt to clarify data obtained from animal models of intimal hyperplasia, we used New Zealand white rabbits, a standardized balloon catheter injury model, and a 0.25% cholesterol supplemented diet. The effects of mechanical injury and hypercholesterolemia separately and combined were determined at the carotid and iliac positions at 12 weeks. En-face planimetry of lesioned intima and measurement of transverse intima-to-media thickness were taken as indices of intimal hyperplasia. No animals received antiplatelet agents or postoperative anticoagulation and all vessels remained patent. Neither procedure alone resulted in statistically significant lesion increase. However, combinations of injury and cholesterol resulted in statistically significant and synergistic lesion enhancement. The quantitative data, coupled with distinctive features noted on scanning electron microscopy and transmission electron microscopy, showed separate and synergistic effects of mechanical injury and cholesterol diet on intimal lesions in this model. Additionally, these effects must be considered in evaluation of animal models of intimal hyperplasia and atherosclerosis. Furthermore, this may help dissect mechanisms of failed revascularizations.
为了阐明从内膜增生动物模型获得的数据，我们使用了新西兰白兔、标准化的球囊导管损伤模型和添加0.25%胆固醇的饮食。分别在12周时在颈动脉和髂动脉位置测定机械损伤和高胆固醇血症单独及联合作用的影响。将病变内膜的正面平面测量和内膜与中膜厚度的横向测量作为内膜增生的指标。没有动物接受抗血小板药物或术后抗凝治疗，所有血管均保持通畅。单独的任何一种操作都不会导致病变在统计学上显著增加。然而，损伤与胆固醇的联合作用导致病变在统计学上显著且协同增强。定量数据，再加上扫描电子显微镜和透射电子显微镜所观察到的独特特征，显示了在该模型中机械损伤和胆固醇饮食对内膜病变的单独及协同作用。此外，在评估内膜增生和动脉粥样硬化动物模型时必须考虑这些作用。此外，这可能有助于剖析血管重建失败的机制。
