速激肽受体拮抗剂对白三烯C_4诱导豚鼠气道收缩和微血管渗漏的作用  

Effects of tachykinin receptor antagonists on leukotriene C 4 induced bronchoconstriction and airway microvascular leakage in guinea pigs 1

作　　者：魏尔清[1] 张纬萍[1] 陆智勇[1] 卞如濂[1] 

机构地区：[1]浙江医科大学药理学教研室神经生物学实验室

出　　处：《中国药理学与毒理学杂志》1997年第1期11-13,共3页Chinese Journal of Pharmacology and Toxicology

基　　金：ABSTRACTTheinvolvementofendogenoustachykininsintheairwayactionsofleukotrieneC4(LTC4)wasstudied.LTC4(0.5μg.kg-1;iv)increasedintrapulmonarypressure(IPP)andextravasationofEvansblueintheairwaysinguineapigs.CP-96345{(2S;3S)-cis-2-(dipheny

摘　　要：本实验探讨了内源性速激肽是否参与白三烯Ｃ４（ＬＴＣ４）的气道效应．ＬＴＣ４（０．５μｇｋｇ－１，ｉｖ）可增高豚鼠肺内压（ＩＰＰ）和气道内依文思蓝渗出。速激肽ＮＫ－１受体拮抗剂ＣＰ－９６３４５｛（２Ｓ，３Ｓ）－顺式－２－（二苯甲基）－Ｎ－［（２－甲氧苯）－甲基］－１－杂氮双环［２．２．２］辛烷－３－胺｝１ｍｇｋｇ－１，ｉｖ，可减弱ＬＴＣ４诱导的依文思蓝渗出；ＮＫ－２受体拮抗剂ＳＲ－４８９６８｛（Ｓ）－Ｎ－甲基－Ｎ－［４－（４－乙酰氨基－４－苯基哌啶）－２－（３，４－二氯苯基）丁基］苯甲酰胺｝，１ｍｇｋｇ－１，ｉｖ，可抑制ＩＰＰ的增高．白三烯拮抗剂ＯＮＯ－１０７８（０．０３ｍｇｋｇ－１，ｉｖ）可阻断这两种反应．结果说明内源性速激肽增强ＬＴＣ４的气道作用，其中ＮＫ－１受体介导微血管渗漏，ＮＫ－２受体介导支气管收缩．The involvement of endogenous tachykinins in the airway actions of leukotriene C 4 (LTC 4) was studied. LTC 4 (0.5 μg·kg 1 , iv) increased intrapulmonary pressure (IPP) and extravasation of Evans blue in the airways in guinea pigs. CP 96345 {(2S,3S) cis 2 (diphenylmethyl) N [(2 methoxyphenyl) methyl] 1 azabicyclooctane 3 amine}, a NK 1 tachykinin receptor antagonist (1 mg·kg 1 , iv) attenuated LTC 4 induced increase of Evans blue extravasation in the airways, and SR 48968 {(S) N methyl N [4 (4 acetylamino 4 phenylpiperidino) 2 (3,4 dichloro phenyl) butyl] benzamide}, a NK 2 receptor antagonist (1 mg·kg 1 , iv) inhibited increase in IPP, respectively. ONO 1078 (0.03 mg·kg 1 , iv), a leukotriene antagonist, decreased both responses. The results indicate that endogenous tachykinins potentiate the responses of LTC 4 on airways, microvascular leakage mediated by NK 1 receptors, and bronchoconstriction by NK 2 receptors.

关 键 词：白三烯 支气管收缩 微血管渗漏性 速激肽 拮抗剂 

分 类 号：R977.4[医药卫生—药品]