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氮芥 - N - 氧化物给药后内淋巴直流电位降低机制的实验研究

Experimental study of the mechanism of the decrease in endocochlear d.c. potential after administration of nitrogen mustard-N-oxide.

作者信息

Asakuma S, Yoshida M, Toriya Y, Hirashima K

出版信息

Acta Otolaryngol. 1984 Mar-Apr;97(3-4):273-82. doi: 10.3109/00016488409130989.

Abstract

20 mg/kg of body weight of nitrogen mustard-N-oxide hydrochloride ( NMNO ) causes a transient decrease in the magnitude of the endocochlear d.c. potential (EP) in the same manner as does nitrogen mustard (NM). NMNO does not, however, change the electrical resistance of the cochlear partition. When the administered dose of NMNO is increased to 40, 60 and 80 mg/kg body weight, a corresponding diminution in the EP is not observed. No ultrastructural changes in the stria vascularis are observed, even in animals administered 80 mg/kg body weight. The reduction of the EP with NMNO could not be attributed to a loss of the electrical insulator effect of the cochlear partition, or to a functional derangement of the stria vascularis. In the experimental animals whose organ of Corti was already destroyed with kanamycin sulfate (KM), NMNO did not reduce the magnitude of the EP. The organ of Corti may be central in understanding the mechanism of NMNO -induced reduction of the EP.

摘要

20毫克/千克体重的盐酸氮芥-N-氧化物(NMNO)会使内耳蜗直流电位(EP)的幅度出现短暂下降,其方式与氮芥(NM)相同。然而,NMNO不会改变耳蜗隔板的电阻。当NMNO的给药剂量增加到40、60和80毫克/千克体重时,未观察到EP相应降低。即使在给予80毫克/千克体重的动物中,也未观察到血管纹有超微结构变化。NMNO导致的EP降低不能归因于耳蜗隔板电绝缘效应的丧失,也不能归因于血管纹的功能紊乱。在柯蒂氏器已被硫酸卡那霉素(KM)破坏的实验动物中,NMNO并未降低EP的幅度。柯蒂氏器可能是理解NMNO诱导的EP降低机制的核心。

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