Erythrocytosis, glomerulomegaly, mesangial hyperplasia, sialyl hyperplasia, and arteriosclerosis induced in rats by nickel subsulfide.

K S McCully, L A Rinehimer, C G Gillies, S M Hopfer, F W Sunderman
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引用次数: 4

Abstract

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.

亚硫化镍致大鼠红细胞增多、肾小球增大、系膜增生、唾液增生及动脉硬化。
各组雄性Fischer大鼠单侧肾内注射亚硫化镍(2.5或5 mg Ni3S2/大鼠)后,每隔1 h至18周处死,进行组织病理学检查。与既往研究结果一致,ni3s2治疗后2 ~ 18周出现骨髓和脾脏红细胞增生,红细胞增多明显。迄今未报道的ni3s2治疗效果包括:(a)双肾肾小球明显肿大和系膜细胞增生;(b)下颌下唾液腺增生,(c)广泛的动脉硬化病变。本研究提示肾小球系膜细胞产生促红细胞生成素。ir注射Ni3S2诱导大鼠动脉硬化病变的发现,为探讨动脉硬化的发病机制提供了新的实验模型。
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