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儿茶酚胺诱导的肌无力。

Catecholamine-induced muscle weakness.

作者信息

Felmus M T, Patten B M, Hart A, Martinez C

出版信息

Arch Neurol. 1977 May;34(5):280-4. doi: 10.1001/archneur.1977.00500170034005.

Abstract

Infusions of epinephrine or levarterenol bitartrate into a rabbit nerve-muscle preparation decreased the force of the evoked twitch of anterior tibial and gastrocnemius-soleus muscles. The adverse effect of the catecholamines was not directly on skeletal muscle. The alpha-receptor blocking drug phenoxybenzamine hydrochloride prevented the adverse effect of the catecholamines if it was given prior to catecholamine infusions and unmasked a weak augmentation of twitch tension. Taken with the finding of abnormal accumulation of catecholamine in human dystrophic muscles, the production of an experimental myopathy resembling human dystrophy by the monoamine oxidase inhibitor pargyline hydrochloride, and the finding of excessive levels of catecholamines in the tissues and urine of dystrophic animals, these experiments support the hypothesis that catecholamines could play a pathogenetic role in some dystrophic diseases of muscle.

摘要

将肾上腺素或重酒石酸去甲肾上腺素注入兔神经 - 肌肉标本中,会降低胫前肌和腓肠肌 - 比目鱼肌诱发抽搐的力量。儿茶酚胺的不良反应并非直接作用于骨骼肌。α受体阻断药物盐酸酚苄明如果在注入儿茶酚胺之前给药,可预防儿茶酚胺的不良反应,并揭示出抽搐张力的微弱增强。结合人类营养不良性肌肉中儿茶酚胺异常蓄积的发现、盐酸优降宁(一种单胺氧化酶抑制剂)产生类似人类营养不良的实验性肌病的发现,以及营养不良动物组织和尿液中儿茶酚胺水平过高的发现,这些实验支持了儿茶酚胺可能在某些肌肉营养不良性疾病中起致病作用这一假说。

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