Sun J, Sakamoto T, Chung K F
Department of Thoracic Medicine, National Heart and Lung Institute, London, UK.
Thorax. 1995 Aug;50(8):875-9. doi: 10.1136/thx.50.8.875.
Sodium metabisulphite (MBS) is known to induce bronchoconstriction in asthmatic patients. The effects of MBS on guinea pig airway smooth muscle and on neurally mediated contraction in vitro have been examined.
Tracheal and bronchial airway segments were placed in oxygenated buffer solution and electrical field stimulation was performed in the presence of indomethacin (10(-5) M) and propranolol (10(-6) M) for the measurement of isometric tension. Atropine (10(-6) M) was added to bronchial tissues.
Concentrations of MBS up to 10(-3) M had no direct effect on airway smooth muscle contraction and did not alter either tracheal smooth muscle contraction induced by electrical field stimulation at all frequencies or acetylcholine-induced tracheal smooth muscle contraction. There was a similar response in the absence of epithelium, except for potentiation of the response induced by electrical field stimulation at 0.5 Hz (24 (10)% increase). However, MBS (10(-5), 10(-6) and 10(-7) M) augmented neurally-mediated non-adrenergic non-cholinergic contractile responses in the bronchi (13.3 (3.2)%, 23.8 (9.6)%, and 6.4 (1.6)%, respectively). MBS had no effect on the contractile response induced by substance P, but at higher concentrations (10(-3) M and 10(-4) M) it caused a time-dependent attenuation of responses induced by either electrical field stimulation or exogenously applied acetylcholine or substance P.
MBS had no direct contractile responses but enhanced bronchoconstriction induced by activation of non-cholinergic neural pathways in the bronchus, probably through increased release of neuropeptides. At high concentrations MBS inhibited contractile responses initiated by receptor or neural stimulation.
已知焦亚硫酸钠（MBS）可诱发哮喘患者支气管收缩。已研究了MBS对豚鼠气道平滑肌及体外神经介导收缩的影响。
将气管和支气管气道段置于含氧缓冲溶液中，并在吲哚美辛（10⁻⁵ M）和普萘洛尔（10⁻⁶ M）存在的情况下进行电场刺激，以测量等长张力。向支气管组织中加入阿托品（10⁻⁶ M）。
浓度高达10⁻³ M的MBS对气道平滑肌收缩无直接影响，且不改变任何频率下电场刺激诱导的气管平滑肌收缩或乙酰胆碱诱导的气管平滑肌收缩。在无上皮的情况下有类似反应，但0.5 Hz电场刺激诱导的反应增强（增加24（10）%）。然而，MBS（10⁻⁵、10⁻⁶和10⁻⁷ M）增强了支气管中神经介导的非肾上腺素能非胆碱能收缩反应（分别为13.3（3.2）%﹑23.8（9.6）%和6.4（1.6）%）。MBS对P物质诱导的收缩反应无影响，但在较高浓度（10⁻³ M和10⁻⁴ M）时，它会导致电场刺激或外源性应用乙酰胆碱或P物质诱导的反应随时间衰减。
MBS无直接收缩反应，但可能通过增加神经肽释放增强支气管中非胆碱能神经通路激活诱导的支气管收缩。在高浓度时，MBS抑制由受体或神经刺激引发的收缩反应。
