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α兴奋剂和β阻滞剂对育亨宾毒性的影响。

Influence of alpha stimulants and beta blockers on yohimbine toxicity.

作者信息

Bourin M, Malinge M, Colombel M C, Larousse C

机构信息

Laboratory of Pharmacology, Faculty of Medicine, Nantes, France.

出版信息

Prog Neuropsychopharmacol Biol Psychiatry. 1988;12(5):569-74. doi: 10.1016/0278-5846(88)90002-4.

Abstract
  1. Potentiation of yohimbine-induced sublethality has been largely used to predict antidepressant action. 2. Several products were tested in order to understand the mechanism of this toxicity better: an alpha-1 central stimulant (adrafinil); an alpha-2 central stimulant (clonidine); and 4 beta-blockers (propranolol, atenolol, penbutolol and metoprolol). 3. It was found that atenolol and adrafinil could not antagonize toxicity, whereas clonidine and the other 3 beta-blockers could. 4. It is suggested that a central beta-origin toxicity exists since only beta-blockers which cross the blood-brain barrier are capable of antagonizing this activity. 5. The fact that clonidine also antagonized this toxicity may be explained by the beta-antagonist action of this substance at the high doses used.
摘要
  1. 育亨宾诱导的亚致死性增强已被广泛用于预测抗抑郁作用。2. 为了更好地理解这种毒性的机制,对几种产品进行了测试:一种α-1中枢兴奋剂(阿屈非尼);一种α-2中枢兴奋剂(可乐定);以及4种β受体阻滞剂(普萘洛尔、阿替洛尔、喷布洛尔和美托洛尔)。3. 发现阿替洛尔和阿屈非尼不能拮抗毒性,而可乐定和其他3种β受体阻滞剂可以。4. 有人提出存在一种中枢β源毒性,因为只有能穿过血脑屏障的β受体阻滞剂才能够拮抗这种活性。5. 可乐定也能拮抗这种毒性这一事实,可能是由于该物质在所用高剂量时的β拮抗作用。

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