McCully K S, Rinehimer L A, Gillies C G, Hopfer S M, Sunderman F W
Virchows Arch A Pathol Anat Histol. 1982;394(3):207-20. doi: 10.1007/BF00430666.
Histopathological examinations were performed upon groups of male Fischer rats killed at intervals from 1 h to 18 weeks after unilateral intrarenal (ir) injection of nickel subsulfide (2.5 or 5 mg of Ni3S2/rat). Consistent with previous findings, erythroid hyperplasia of bone marrow and spleen occurred from 2 to 18 weeks after Ni3S2-treatment, resulting in pronounced erythrocytosis. Hitherto unreported effects of Ni3S2-treatment include: (a) marked glomerulomegaly and hyperplasia of mesangial cells in both kidneys; (b) hyperplasia of submandibular salivary glands, and (c) widespread arteriosclerotic lesions. The present study suggests that mesangial cells of renal glomeruli produce erythropoietin. Discovery that ir injection of Ni3S2 induces arteriosclerotic lesions in rats furnishes a new experimental model to investigate the pathogenesis of arteriosclerosis.
对单侧肾内（ir）注射硫化镍（2.5或5mg Ni3S2/大鼠）后1小时至18周内不同时间点处死的雄性Fischer大鼠组进行了组织病理学检查。与先前的研究结果一致，在Ni3S2处理后2至18周出现骨髓和脾脏的红细胞增生，导致明显的红细胞增多症。Ni3S2处理迄今未报告的影响包括：（a）双侧肾脏肾小球显著肿大和系膜细胞增生；（b）下颌下唾液腺增生，以及（c）广泛的动脉粥样硬化病变。本研究表明肾小球系膜细胞产生促红细胞生成素。发现ir注射Ni3S2可诱导大鼠动脉粥样硬化病变，为研究动脉粥样硬化的发病机制提供了一个新的实验模型。
