Hampton J A, Bernardo D A, Khan N A, Lacher D A, Rapp J P, Gohara A F, Goldblatt P J
Department of Pathology, Medical College of Ohio, Toledo.
Lab Invest. 1989 Jun;60(6):839-46.
The progression of small vessel renal vascular disease was studied in inbred Dahl salt-sensitive (SS/Jr) and salt-resistant rats with acute hypertension induced by a high salt diet. Corrected cross-sectional areas of wall (WAC) and lumen were measured by planimetry and histologic staining for fibrin, hyalin deposition, and elastic lamellae was performed. In SS/Jr rats on the high salt diet, the hallmarks of malignant hypertension (fibrinoid necrosis, hyperplastic and necrotizing arteritis) appeared by week 2 and were intensified after 4 weeks on the high salt diet. Renal vascular lesions from SS/Jr rats were characterized by: hyperplasia and/or hypertrophy of medial smooth muscle cells; intimal proliferation; fibrin, basophilic mucoid, and hyalin deposition within the the subendothelial space and media; variable adventitial fibrosis; and accumulation of mononuclear inflammatory cells in the adventitia and media. Interlobular arteries from both rat strains exhibited significantly increased cross-sectional areas over time for all measured parameters. Intralobular arterioles from both rat strains exhibited significantly increased cross-sectional areas over time for all measured parameters except lumen from SS/Jr rats. For SS/Jr rats, increased WAC from both arterial divisions correlated positively with systolic blood pressure, but not body weight. In salt-resistant rats, increased WAC from both arterial divisions correlated positively with body weight, but not systolic blood pressure. We concluded that the rapid increase in WAC from SS/Jr rats could not be attributed solely to the normal growth of the rat. With the development of acute hypertension in the SS/Jr rat, these results demonstrate the potential usefulness of this model to investigate the pathogenesis of similar renal vascular alterations which are observed in man.
在通过高盐饮食诱导急性高血压的近交系Dahl盐敏感(SS/Jr)大鼠和盐抵抗大鼠中,研究了小血管肾血管疾病的进展情况。通过平面测量法测量壁(WAC)和管腔的校正横截面积,并对纤维蛋白、透明质沉积进行组织学染色,同时观察弹性板情况。在高盐饮食的SS/Jr大鼠中,恶性高血压的特征(纤维蛋白样坏死、增生性和坏死性动脉炎)在第2周出现,并在高盐饮食4周后加剧。SS/Jr大鼠的肾血管病变特征为:中膜平滑肌细胞增生和/或肥大;内膜增生;内皮下间隙和中膜内有纤维蛋白、嗜碱性黏液样物质和透明质沉积;外膜纤维化程度不一;外膜和中膜有单核炎性细胞积聚。随着时间推移,两种大鼠品系的小叶间动脉所有测量参数的横截面积均显著增加。两种大鼠品系的小叶内小动脉,除SS/Jr大鼠的管腔外,所有测量参数的横截面积均随时间显著增加。对于SS/Jr大鼠,两个动脉分支的WAC增加与收缩压呈正相关,但与体重无关。在盐抵抗大鼠中,两个动脉分支的WAC增加与体重呈正相关,但与收缩压无关。我们得出结论,SS/Jr大鼠WAC的快速增加不能仅归因于大鼠的正常生长。随着SS/Jr大鼠急性高血压的发展,这些结果表明该模型在研究人类中观察到的类似肾血管改变的发病机制方面具有潜在的实用性。