N-ω-硝基-L-精氨酸甲酯可预防他克林诱导的氯化锂处理大鼠的癫痫发作和脑损伤。

Tacrine-induced seizures and brain damage in LiCl-treated rats can be prevented by N omega-nitro-L-arginine methyl ester.

作者信息

Bagetta G, Iannone M, Scorsa A M, Nisticò G

机构信息

Department of Biology, University of Rome Tor Vergata, Italy.

出版信息

Eur J Pharmacol. 1992 Mar 24;213(2):301-4. doi: 10.1016/0014-2999(92)90695-z.

DOI:10.1016/0014-2999(92)90695-z

PMID:1325916

Abstract

The effects of tacrine (5 mg/kg i.p.), a potent acetylcholinesterase inhibitor, were studied in rats pretreated (24 h beforehand) with a single dose (12 mEq/kg i.p.) of LiCl. Tacrine and LiCl were ineffective when given individually. Tacrine elicited seizures and brain damage in 90% of the rats treated. The intracerebroventricular microinfusion of N omega-nitro-L-arginine methyl ester (300 micrograms given 24 h after LiCl administration) significantly reduced the seizures and brain damage produced by tacrine (given 15 min later). These experiments suggest that the seizures and brain damage elicited by tacrine may be due, in part, to increased nitric oxide production in the brain.

摘要

在预先（提前24小时）用单剂量（12毫当量/千克腹腔注射）氯化锂处理的大鼠中，研究了强效乙酰胆碱酯酶抑制剂他克林（5毫克/千克腹腔注射）的作用。单独给予他克林和氯化锂时均无效。他克林诱发了90%接受治疗大鼠的癫痫发作和脑损伤。在氯化锂给药24小时后经脑室内微量注射N-硝基-L-精氨酸甲酯（给予300微克）显著减少了他克林（15分钟后给予）所产生的癫痫发作和脑损伤。这些实验表明，他克林引发的癫痫发作和脑损伤可能部分归因于大脑中一氧化氮生成增加。