Tamaoki J, Kondo M, Takemura H, Chiyotani A, Tagaya E, Konno K
First Department of Medicine, Tokyo Women's Medical College, Japan.
Nihon Kyobu Shikkan Gakkai Zasshi. 1994 Dec;32(12):1164-9.
There is increasing evidence that nitric oxide (NO) plays a role in the regulation of airway and vascular smooth muscle tone, pulmonary microvascular permeability, and host defense. However, it remains uncertain whether NO is actually released from airway mucosa. We therefore directly measured NO concentrations in the perfusate of rabbit tracheal mucosal surface, with an NO-selective electrode. The electrode was made of Pt/Ir alloy coated with a three-layered membrane that consisted of KCl, No-selective silicone resin, and a normal silicone membrane. Termination of tracheal perfusion with Krebs-Henseleit solution increased the electrical current derived from oxidation of NO at the electrode, and reperfusion rapidly decreased the current to the baseline value. Addition of L-NG-arginine methylester (L-NAME, 10(-3) M) to the perfusate decreased NO release, but D-NAME had no effect. Subsequent addition of L-arginine (10(-3) M) reversed the inhibition by L-NAME and greatly increased NO release above the baseline value. Histochemical staining to reveal NADPH diaphorase activity in the tracheal tissue showed a strong blue reaction mainly in the epithelial cells. These results suggest that NO is continuously released in the airway mucosal surface, probably from the epithelial cells rich in NO synthase.
越来越多的证据表明，一氧化氮（NO）在气道和血管平滑肌张力、肺微血管通透性及宿主防御的调节中发挥作用。然而，NO是否实际从气道黏膜释放仍不确定。因此，我们用NO选择性电极直接测量了兔气管黏膜表面灌流液中的NO浓度。该电极由涂有三层膜的铂/铱合金制成，这三层膜分别为氯化钾、NO选择性硅树脂和普通硅膜。用Krebs-Henseleit溶液终止气管灌流会增加电极处因NO氧化产生的电流，而再灌注会使电流迅速降至基线值。向灌流液中添加L-NG-精氨酸甲酯（L-NAME，10⁻³ M）会减少NO释放，但D-NAME无此作用。随后添加L-精氨酸（10⁻³ M）可逆转L-NAME的抑制作用，并使NO释放量大幅增加至基线值以上。用于显示气管组织中NADPH黄递酶活性的组织化学染色显示，主要在上皮细胞中有强烈的蓝色反应。这些结果表明，NO在气道黏膜表面持续释放，可能来自富含一氧化氮合酶的上皮细胞。
