Nagornev V A, Bobryshev Iu V, Ivanovskiĭ Iu V
Arkh Patol. 1982;44(10):54-60.
The development of experimental atherosclerosis in rabbits is accompanied by infiltration into the aorta intima of low density lipoproteins and marked proliferation of smooth muscle cells. The activated smooth muscle cells take part in desmoplastic reactions being the main source of collagen synthesized in atherosclerotic plaques. Outgrowth of the connective tissue in the zone of the elastic membrane fenestration leads to disturbance of the outflow of plasma components and causes edema of the intima. It is assumed that an atherosclerotically altered vascular wall may synthesize collagen with abnormal antigenic structure acquiring autoantigenic properties.
家兔实验性动脉粥样硬化的发展伴随着低密度脂蛋白浸润至主动脉内膜以及平滑肌细胞的显著增殖。活化的平滑肌细胞参与形成结缔组织增生反应,是动脉粥样硬化斑块中合成胶原蛋白的主要来源。弹性膜窗区结缔组织的增生导致血浆成分流出受阻,引起内膜水肿。据推测,发生动脉粥样硬化改变的血管壁可能合成具有异常抗原结构并获得自身抗原特性的胶原蛋白。