Newball H H, Lenfant C
Respir Physiol. 1977 Jun;30(1-2):125-36. doi: 10.1016/0034-5687(77)90026-3.
The mechanism of prostaglandin F2 alpha(PGF2alpha)-induced airway constriction was explored by determining the influence of atropine and cromolyn on the bronchoconstrictive properties of PGF2alpha. Increasing doses of aerosolized PGF2alpha were given (150, 300, 600, 1200 microgram) and the response of subjects was determined by measurements of spirometry, specific airway conductance (SGaw), and closing volumes. In normal subjects, PGF2alpha induced small but significant decreases of SGaw and spirometric parameters (FVC, FEV1), whereas there was no effect on the closing volumes. In contrast, in asthmatics, PGF2 alpha induced large decreases of SGaw and spirometric parameters. Asthmatics experienced severe and prolonged shortness of breath and wheezing, whereas normal controls experienced neither. Neither atropine nor atropine plus cromolyn was capable of preventing or substantially reversing the PGF2alpha-induced symptoms and airway constriction. The data suggest that reflex bronchoconstriction via irritant receptors is not a major mechanism of PGF2alpha-induced airway constriction. Although a minor vagally mediated reflex component may participate in the PGF2alpha-induced bronchoconstriction, it is masked by an overwhelming non-reflex mechanism that is probably a direct constricting effect of airways smooth muscle that is exquisitely sensitive to PGF2alpha.
通过测定阿托品和色甘酸钠对前列腺素F2α（PGF2α）诱导的气道收缩特性的影响，探讨了PGF2α诱导气道收缩的机制。给予递增剂量的雾化PGF2α（150、300、600、1200微克），并通过测量肺量计、比气道传导率（SGaw）和闭合气量来确定受试者的反应。在正常受试者中，PGF2α引起SGaw和肺量计参数（FVC、FEV1）小幅但显著下降，而对闭合气量无影响。相比之下，在哮喘患者中，PGF2α引起SGaw和肺量计参数大幅下降。哮喘患者出现严重且持续时间长的呼吸急促和喘息，而正常对照组则无此现象。阿托品以及阿托品加色甘酸钠均不能预防或显著逆转PGF2α诱导的症状和气道收缩。数据表明，通过刺激感受器引起的反射性支气管收缩不是PGF2α诱导气道收缩的主要机制。虽然可能有轻微的迷走神经介导的反射成分参与PGF2α诱导的支气管收缩，但它被一种压倒性的非反射机制所掩盖，这种机制可能是气道平滑肌对PGF2α极度敏感的直接收缩作用。
