Hoshi A, Kobayashi J, Kitamura S
Department of Pulmonary Medicine, Jichi Medical School, Tochigi, Japan.
Nihon Kyobu Shikkan Gakkai Zasshi. 1992 Jun;30(6):1091-6.
Various kinds of chemical mediators have been implicated in the pathogenesis of bronchial asthma. PGD2 is a cyclooxygenase product which has various physiological effects. In this experimental study, we investigated the role of PGD2 in the pathogenesis of bronchial asthma. In a bioassay system, PGD2 caused dose-dependent contractile responses in non-sensitized guinea pig trachea and lung tissue strips. The subthreshold concentration of PGD2 in both strips was 25 ng/ml. Acetylcholine-induced contractile responses in both strips were significantly increased by continuous infusion of PGD2. In the experimental model of bronchial asthma, the levels of PGD2 were significantly increased in serum, bronchoalveolar lavage fluid (BALF) and lung tissue of sensitized guinea pigs after antigen challenge. We have also reported that the levels of PGD2 in BALF were elevated in patients with stable state bronchial asthma. These results suggest that PGD2 may be a key substance that increases airway responsiveness and induces asthmatic attacks.
多种化学介质与支气管哮喘的发病机制有关。前列腺素D2（PGD2）是一种具有多种生理效应的环氧化酶产物。在本实验研究中，我们调查了PGD2在支气管哮喘发病机制中的作用。在生物测定系统中，PGD2在未致敏的豚鼠气管和肺组织条带中引起剂量依赖性收缩反应。两条带中PGD2的阈下浓度均为25 ng/ml。通过持续输注PGD2，两条带中乙酰胆碱诱导的收缩反应均显著增加。在支气管哮喘实验模型中，致敏豚鼠在抗原激发后，血清、支气管肺泡灌洗液（BALF）和肺组织中PGD2水平显著升高。我们还报道，稳定期支气管哮喘患者BALF中PGD2水平升高。这些结果表明，PGD2可能是增加气道反应性并诱发哮喘发作的关键物质。
