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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．
This experiment explored whether endogenous tachykinins are involved in the airway effects of leukotriene C4 (LTC4). LTC4 (0.5μgkg-1, iv) increased intrapulmonary pressure (IPP) and Evans blue exudate in guinea pigs. Tachykinin NK-1 receptor antagonist CP-96345 {(2S, 3S) -cis-2- (diphenylmethyl) -N - [(2-methoxyphenyl) -methyl] 1mgkg-1, iv can reduce LTC4-induced Evans blue exudation; NK-2 receptor antagonist SR-48968 {(S) -N- Methyl-N- [4- (4-acetylamino-4-phenylpiperidine) -2- (3,4- dichlorophenyl) butyl] benzamide}, 1 mg kg -1, iv, Increased IPP. The leukotriene antagonist ONO-1078 (0.03 mg kg-1, iv) blocked both reactions. The results suggest that endogenous tachykinins enhance the airway effects of LTC4, with NK-1 receptor mediating microvascular leakage and NK-2 receptor-mediated bronchoconstriction.