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血管加压素可能介导热性惊厥。

Vasopressin may mediate febrile convulsions.

作者信息

Kasting N W, Veale W L, Cooper K E, Lederis K

出版信息

Brain Res. 1981 Jun 1;213(2):327-33. doi: 10.1016/0006-8993(81)90238-9.

Abstract

The possibility that arginine vasopressin (AVP) is involved in the etiology of febrile convulsions was investigated by experiments on hyperthermia-induced convulsions in rats. Homozygous Brattleboro rats, which genetically lack AVP, and Long Evans rats, which were passively immunized by intracerebroventricular anti-AVP antiserum, either convulsed at higher body temperatures than untreated Long Evans rats or did not convulse at all. This indicates that a lack of AVP increases the threshold for the convulsions. High blood levels of AVP in hyperthermic convulsing rats compared to hyperthermic non-convulsive rats support the hypothesis that AVP may mediate febrile convulsions.

摘要

通过对大鼠热诱导惊厥进行实验,研究了精氨酸加压素(AVP)参与热性惊厥病因的可能性。遗传性缺乏AVP的纯合布拉特洛维大鼠,以及经脑室内注射抗AVP抗血清进行被动免疫的朗·埃文斯大鼠,要么在比未处理的朗·埃文斯大鼠更高的体温下惊厥,要么根本不发生惊厥。这表明AVP的缺乏会提高惊厥阈值。与热诱导非惊厥大鼠相比,热诱导惊厥大鼠的AVP血药浓度高,这支持了AVP可能介导热性惊厥的假说。

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