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脑室内注射纳洛酮对过敏性休克的有益作用是通过外周β-肾上腺素能机制介导的。

Beneficial effect of i.c.v. naloxone in anaphylactic shock is mediated through peripheral beta-adrenoceptive mechanisms.

作者信息

Amir S

出版信息

Brain Res. 1984 Jan 2;290(1):191-4. doi: 10.1016/0006-8993(84)90754-6.

Abstract

Intracerebroventricular (i.c.v.) administration of 10 micrograms naloxone significantly improved survival following experimental anaphylaxis in mice. The protective effect of i.c.v. naloxone was reversed by treatments which disrupted sympathetic outflow to the adrenal medulla, i.e. ganglionic blockade by chorisondamine chloride or denervation of the adrenal glands or by inhibition of beta-adrenoceptive sites by propranolol. These results indicate that naloxone's beneficial effect in anaphylactic shock involves central actions which are peripherally mediated through activation of beta-adrenoceptive mechanisms.

摘要

脑室内(i.c.v.)注射10微克纳洛酮可显著提高小鼠实验性过敏反应后的存活率。破坏交感神经向肾上腺髓质的传出通路的处理可逆转脑室内注射纳洛酮的保护作用,即通过氯化氯异吲哚铵进行神经节阻断、肾上腺去神经支配或通过普萘洛尔抑制β-肾上腺素能位点。这些结果表明,纳洛酮在过敏性休克中的有益作用涉及中枢作用,这些中枢作用通过β-肾上腺素能机制的激活在外周介导。

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