Yoshihara S, Geppetti P, Lindén A, Hara M, Chan B, Nadel J A
Cardiovascular Research Institute, University of California San Francisco 94143-0130, USA.
J Allergy Clin Immunol. 1996 Mar;97(3):756-60. doi: 10.1016/s0091-6749(96)80152-7.
The role of tachykinins in the potentiation of antigen-evoked bronchoconstriction induced by inhalation of cold air was studied in guinea pigs. Cold air was delivered through a tracheal cannula to anesthetized, artificially ventilated guinea pigs sensitized with ovalbumin and pretreated with atropine (1.4 micromol/kg). Inhalation of cold air increased total pulmonary resistance (RL) in a time-dependent manner; inhalation of cold air for 10 or 15 minutes, but not for 5 minutes, produced a significant increase in RL. Aerosolized ovalbumin (5 breaths) increased RL in a dose-dependent manner (0.5% to 5%). Inhalation of cold air for 5 minutes significantly enhanced both the peak and the duration of the increase in RL induced by 0.5% ovalbumin. The tachykinin neurokinin 2-receptor antagonist, SR 48968 (0.3 micromol/kg intravenously) inhibited both the peak and the duration of the bronchoconstriction induced by 5-minute inhalation of cold air and ovalbumin (0.5%), whereas it did not affect the response to ovalbumin (0.5%) alone. These findings suggest that exposure to cold air potentiates the bronchoconstriction response to antigen and that this potentiation is mediated by tachykinin release from sensory nerves.
在豚鼠中研究了速激肽在吸入冷空气诱导的抗原激发支气管收缩增强中的作用。通过气管插管将冷空气输送给用卵清蛋白致敏并预先用阿托品（1.4微摩尔/千克）处理的麻醉、人工通气的豚鼠。吸入冷空气以时间依赖性方式增加总肺阻力（RL）；吸入冷空气10或15分钟可使RL显著增加，但吸入5分钟则不会。雾化的卵清蛋白（5次呼吸）以剂量依赖性方式（0.5%至5%）增加RL。吸入冷空气5分钟显著增强了0.5%卵清蛋白诱导的RL增加的峰值和持续时间。速激肽神经激肽2受体拮抗剂SR 48968（静脉注射0.3微摩尔/千克）抑制了吸入冷空气5分钟和卵清蛋白（0.5%）诱导的支气管收缩的峰值和持续时间，而它对单独卵清蛋白（0.5%）的反应没有影响。这些发现表明，暴露于冷空气会增强对抗原的支气管收缩反应，并且这种增强是由感觉神经释放的速激肽介导的。
