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镉在动物模型高血压中的病因学作用。

Etiological role of cadmium in hypertension in an animal model.

作者信息

Ohanian E V, Iwai J

出版信息

J Environ Pathol Toxicol. 1980 Sep;4(2-3):229-41.

PMID:7462901
Abstract

Dahl hypertension-resistant (R) and hypertension-sensitive (S) lines of rats were used to determine whether cadmium plays an etiological role in hypertension. In Study I, weanling (3-week-old) R and S rats of both sexes were given a low-salt (0.4% NaCl) diet and were divided into two groups. Rats in the cadmium group were injected with cadmium (2 mg/kg body weight, ip), whereas the controls received identical volumes of saline. Three weeks after the first injection, no elevations of systolic blood pressure were detected. A second dose of cadmium (1 mg/kg) produced hypertension in S females but not in S males or in R rats of either sex. Also, female S cadmium rats manifested significant (p less than 0.01) mild to moderate renal vascular changes. The concentrations of cadmium in hepatic and renal tissues of S cadmium rats were significantly higher (p less than 0.001) than in R rats. In Study II, weanling (3-week-old) female S rats on a high-salt (4% NaCl) diet were given cadmium (2 mg/kg body weight, ip) at week 3 followed by second and third injections of cadmium (1 mg/kg) at weeks 6 and 23. S controls received the same volumes of saline. Cadmium enhanced the rate and the degree of salt-induced hypertension development. Pathological lesions of periarteritis nodosa in the mesenteric arteries and renal vascular lesions occurred to the same extent in the cadmium and control groups. These data indicate that differences in genetic background influence the development of cadmium-induced hypertension in weanling rats, and that cadmium exacerbates the severity of salt-induced hypertension.

摘要

采用 Dahl 高血压抗性(R)和高血压敏感(S)品系大鼠来确定镉是否在高血压病因学中起作用。在研究 I 中,给断奶(3 周龄)的雌雄 R 和 S 大鼠喂食低盐(0.4% NaCl)饮食,并分为两组。镉组大鼠腹腔注射镉(2 mg/kg 体重),而对照组注射相同体积的生理盐水。首次注射三周后,未检测到收缩压升高。第二次注射镉(1 mg/kg)使 S 雌性大鼠出现高血压,但 S 雄性大鼠或任何性别的 R 大鼠均未出现。此外,雌性 S 镉处理大鼠表现出显著(p < 0.01)的轻度至中度肾血管变化。S 镉处理大鼠肝组织和肾组织中的镉浓度显著高于 R 大鼠(p < 0.001)。在研究 II 中,给喂食高盐(4% NaCl)饮食的断奶(3 周龄)雌性 S 大鼠在第 3 周腹腔注射镉(2 mg/kg 体重),随后在第 6 周和第 23 周进行第二次和第三次镉注射(1 mg/kg)。S 对照组注射相同体积的生理盐水。镉加快了盐诱导高血压的发展速度和程度。镉组和对照组肠系膜动脉结节性动脉周围炎的病理病变以及肾血管病变程度相同。这些数据表明,遗传背景差异影响断奶大鼠镉诱导高血压的发展,并且镉会加重盐诱导高血压的严重程度。

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