Nogami H, Umeno E, Kano S, Hirose T, Nishima S
Clinical Research Institute, National Minami Fukuoka Chest Hospital, Japan.
Eur Respir J. 1998 Dec;12(6):1318-21. doi: 10.1183/09031936.98.12061318.
To elucidate the role of endogenous nitric oxide (NO) in allergen- (AIB) and hyperventilation-induced bronchoconstriction (HIB), the effects of an NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), on AIB and HIB were studied in guinea-pigs. In the AIB group, 21 anaesthetized guinea-pigs, actively sensitized with 1% ovalbumin, were challenged with aerosolized 0.1% ovalbumin solution under mechanical ventilation. In the HIB group, 14 guinea-pigs were challenged with hyperventilation (tidal volume of 12 mL x kg(-1) at 150 breaths x min(-1) with 21% O2 and 5% CO2 dry gas) for 5 min. In both groups, lung resistance (RL) was measured using a pressure-volume-sensitive body plethysmograph, with or without L-NAME pretreatment (8 mg x kg(-1) i.v. followed by 2 mg x kg(-1) x min(-1) i.v.). The NO precursor, L-arginine was injected at a rate of 15 mg x kg(-1) x min(-1) after L-NAME injection (10 mg x kg(-1)) in the AIB group. The results were as follows. In the AIB group, the maximal RL change was significantly potentiated by pretreatment with L-NAME. This potentiating effect of L-NAME was reversed by L-arginine. In the HIB group, the pretreatment with L-NAME had no effect on increases in RL. These findings suggest that endogenous nitric oxide may play an important role in the modulation of allergen-, but not hyperventilation-induced bronchoconstriction in guinea-pigs.
为阐明内源性一氧化氮（NO）在变应原诱导的支气管收缩（AIB）和过度通气诱导的支气管收缩（HIB）中的作用，研究了一氧化氮合酶抑制剂NG-硝基-L-精氨酸甲酯（L-NAME）对豚鼠AIB和HIB的影响。在AIB组中，21只经1%卵清蛋白主动致敏的麻醉豚鼠，在机械通气下用雾化的0.1%卵清蛋白溶液进行激发。在HIB组中，14只豚鼠进行5分钟的过度通气（潮气量为12 mL·kg⁻¹，呼吸频率为150次/分钟，吸入21% O₂和5% CO₂的干燥气体）。在两组中，使用压力容积敏感型体容积描记仪测量肺阻力（RL），测量时有无L-NAME预处理（静脉注射8 mg·kg⁻¹，随后以2 mg·kg⁻¹·分钟⁻¹静脉注射）。在AIB组中，在注射L-NAME（10 mg·kg⁻¹）后，以15 mg·kg⁻¹·分钟⁻¹的速率注射NO前体L-精氨酸。结果如下。在AIB组中，L-NAME预处理显著增强了最大RL变化。L-NAME的这种增强作用被L-精氨酸逆转。在HIB组中，L-NAME预处理对RL的增加没有影响。这些发现表明，内源性一氧化氮可能在豚鼠变应原诱导的支气管收缩调节中起重要作用，但在过度通气诱导的支气管收缩调节中不起作用。
