Accinni L, Dixon F J
Am J Pathol. 1979 Aug;96(2):477-92.
The pathogenesis of the degenerative vascular disease and myocardial infarction that develop in mice with lupus-like disease was studied by immunofluorescence, light microscopy, and electron microscopy. Medium and small coronary arteries and arterioles of both infarcted and noninfarcted hearts had focal degenerative lesions consisting of deposits of periodic-acid--Schiff (PAS)-positive or eosinophilic material in the intima and to a lesser extent in the media, degenerative changes in the media without accompanying cellular inflammation, and occasional proliferation or swelling of intimal cells. These lesions often narrowed and, together with platelet aggregation, occasionally occluded the vascular lumens. Granular deposits of mouse immunoglobulin, C3, and occasionally gp70 were present in the walls of medium and small arteries, arterioles, and venules of both infarcted and noninfarcted myocardium. Dense deposits of foreign material were found by electron microscopy in areas corresponding to the immune deposits. These findings are consistent with the interpretation that these noninflammatory vascular lesions are caused by local deposition of antigen--antibody complexes. The immune-complex--mediated injury appears to lead to thrombotic and/or obliterative vascular changes that contribute to decrease of the coronary blood flow and to the development of myocardial infarction.
通过免疫荧光、光学显微镜和电子显微镜研究了患有狼疮样疾病的小鼠发生的退行性血管疾病和心肌梗死的发病机制。梗死和未梗死心脏的中小冠状动脉和小动脉均有局灶性退行性病变，包括内膜中存在高碘酸-希夫（PAS）阳性或嗜酸性物质沉积，中膜也有较轻程度的沉积，中膜有退行性改变但无伴随的细胞炎症，内膜细胞偶尔增殖或肿胀。这些病变常使血管腔狭窄，并与血小板聚集一起偶尔阻塞血管腔。梗死和未梗死心肌的中小动脉、小动脉和小静脉壁中存在小鼠免疫球蛋白、C3颗粒沉积，偶尔还有gp70沉积。通过电子显微镜在与免疫沉积物相对应的区域发现了致密的异物沉积物。这些发现与以下解释一致，即这些非炎症性血管病变是由抗原-抗体复合物的局部沉积引起的。免疫复合物介导的损伤似乎导致血栓形成和/或闭塞性血管改变，这有助于减少冠状动脉血流并促进心肌梗死的发生。
