Barnes P J
Department of Thoracic Medicine, National Heart and Lung Institute, Brompton Hospital, London, United Kingdom.
Drugs. 1989;37 Suppl 1:94-100; discussion 127-36. doi: 10.2165/00003495-198900371-00017.
Microvascular leakage and neurogenic mechanisms may be important components of the inflammatory response in asthmatic airways. We have examined the effects of nedocromil sodium on these responses. In guinea-pig airway, microvascular leakage induced by allergen was significantly inhibited by prior treatment with nedocromil sodium (100 micrograms/kg IV), but this had no effect on histamine-induced leakage and reduced PAF-induced leakage only at a dosage of 5 mg/kg. This suggests that nedocromil sodium acts mainly by preventing the release of inflammatory mediators. Both sulphur dioxide (SO2) and bradykinin cause bronchoconstriction in asthmatic patients, which is likely to be due to a neural mechanism since SO2 activates C-fibre sensory nerve endings in airways. Inhaled nedocromil sodium is effective in inhibiting both SO2- and bradykinin-induced bronchoconstriction, and furthermore reduces the sensation of dyspnoea, indicating a possible action on sensory nerve endings in airways.
微血管渗漏和神经源性机制可能是哮喘气道炎症反应的重要组成部分。我们已经研究了奈多罗米钠对这些反应的影响。在豚鼠气道中，预先用奈多罗米钠（100微克/千克静脉注射）治疗可显著抑制变应原诱导的微血管渗漏，但这对组胺诱导的渗漏没有影响，并且仅在5毫克/千克的剂量下才降低血小板活化因子诱导的渗漏。这表明奈多罗米钠主要通过阻止炎症介质的释放起作用。二氧化硫（SO2）和缓激肽均可引起哮喘患者的支气管收缩，这可能是由于神经机制，因为SO2激活气道中的C纤维感觉神经末梢。吸入奈多罗米钠可有效抑制SO2和缓激肽诱导的支气管收缩，此外还可减轻呼吸困难的感觉，表明其可能作用于气道中的感觉神经末梢。
