Yoshihara S, Geppetti P, Hara M, Linden A, Ricciardolo F L, Chan B, Nadel J A
Cardiovascular Research Institute and Department of Medicine, University of California San Francisco, 94143, USA.
Eur J Pharmacol. 1996 Feb 5;296(3):291-6. doi: 10.1016/0014-2999(95)00719-9.
In the present study, we investigated the role of acetylcholine, tachykinins and kinins in the bronchoconstriction induced by cold air inhalation. Cold air was delivered to anaesthetised, artificially ventilated guinea pigs through a tracheal cannula. Inhalation of cold air increased the maximum total pulmonary resistance (RL) in a time-dependent manner, reaching a maximum after 15 min of exposure. The increase in RL induced by exposure to cold air for 10 min was not affected by pretreatment with atropine (1.4 mu mol/kg, i.v.); it was abolished by the tachykinin NK2 receptor antagonist, SR 48968 (0.3 mu mol/kg, i.v.) and was reduced by 58% by the kinin B2 receptor antagonist, HOE 140 (0.1 mu mol/kg, i.v.). These findings suggest that cold air induces bronchoconstriction in guinea pigs via a cascade that involves the release of kinins and tachykinins.
在本研究中，我们调查了乙酰胆碱、速激肽和激肽在冷空气吸入诱导的支气管收缩中的作用。冷空气通过气管插管输送给麻醉的、人工通气的豚鼠。吸入冷空气以时间依赖性方式增加最大总肺阻力（RL），在暴露15分钟后达到最大值。暴露于冷空气10分钟诱导的RL增加不受阿托品（1.4μmol/kg，静脉注射）预处理的影响；它被速激肽NK2受体拮抗剂SR 48968（0.3μmol/kg，静脉注射）消除，并被激肽B2受体拮抗剂HOE 140（0.1μmol/kg，静脉注射）降低58%。这些发现表明，冷空气通过涉及激肽和速激肽释放的级联反应在豚鼠中诱导支气管收缩。
