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乙醇诱导的心脏肥大:发展与肾上腺儿茶酚胺排泄之间的相关性。

Ethanol-induced cardiac hypertrophy: correlation between development and the excretion of adrenal catecholamines.

作者信息

Adams M A, Hirst M

出版信息

Pharmacol Biochem Behav. 1986 Jan;24(1):33-8. doi: 10.1016/0091-3057(86)90040-7.

Abstract

The progression of cardiac hypertrophy and the effects on adrenal medullary catecholamine content and release were determined in rats given ethanol, in conjunction with a supplementary diet, by gavage, every eight hours for periods up to 96 hours. Ethanol caused a marked depletion of adrenal medullary adrenaline content which fell to about 25 percent of control after the full time course. During this time, there were two- to fourfold increases in urinary noradrenaline content and five- to tenfold increases in urinary adrenaline. Cardiac hypertrophy, with increases in protein content and tissue weight of both ventricles, was evident at 24 hours of intoxication. By 96 hours of treatment these markers had increased more than 20% over control values. Proportional heart weight increases per day correlated significantly with daily urinary catecholamine excretion, providing support for the hypothesis that ethanol induced cardiac hypertrophy in the rat results from catecholaminergic stimulation, primarily of adrenal medullary origin.

摘要

通过每8小时经口灌胃给予大鼠乙醇并搭配补充饮食,持续长达96小时,测定心脏肥大的进展以及对肾上腺髓质儿茶酚胺含量和释放的影响。乙醇导致肾上腺髓质肾上腺素含量显著减少,在整个时间过程结束后降至对照组的约25%。在此期间,尿去甲肾上腺素含量增加了2至4倍,尿肾上腺素增加了5至10倍。在中毒24小时时,心脏肥大明显,两个心室的蛋白质含量和组织重量均增加。到治疗96小时时,这些指标比对照值增加了20%以上。每天心脏重量的增加比例与每日尿儿茶酚胺排泄量显著相关,这为乙醇诱导大鼠心脏肥大是由儿茶酚胺能刺激(主要源于肾上腺髓质)导致的这一假说提供了支持。

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