Melillo E, Woolley K L, Manning P J, Watson R M, O'Byrne P M
Department of Medicine, McMaster University, Hamilton, Ontario, Canada.
Am J Respir Crit Care Med. 1994 May;149(5):1138-41. doi: 10.1164/ajrccm.149.5.8173753.
Previous studies have suggested that the endogenous release of inhibitory prostanoids limits the bronchoconstrictor response to repeated exercise. The aim of our study was to determine whether inhaled prostaglandin (PG)E2 attenuates exercise-induced bronchoconstriction or methacholine airway responsiveness in asthmatic subjects. Eight subjects with mild stable asthma and exercise bronchoconstriction were studied on 4 separate days, 48 h apart. Subjects inhaled PGE2 or placebo in a randomized, crossover, double-blind fashion, 30 min prior to an exercise challenge or a methacholine challenge. PGE2 inhalation significantly attenuated exercise bronchoconstriction. The mean maximal %fall in FEV1 after exercise was 26% (SEM 3.7%) after placebo, and was 9.7% (SEM 2.7%) after PGE2 (p < 0.001). PGE2 also significantly reduced the duration of exercise bronchoconstriction (p = 0.034). However, PGE2 did not significantly attenuate methacholine airway responsiveness. The geometric mean methacholine provocative concentration causing a 20% fall in FEV1 (PC20) was 0.77 (%SEM 1.48) after placebo day, and 1.41 (%SEM 2.20) after PGE2 (p = 0.30). These results demonstrate that inhaled PGE2 markedly attenuates exercise bronchoconstriction in asthmatic subjects and suggest that this effect is not occurring through functional antagonism of airway smooth muscle.
以往研究表明，抑制性前列腺素的内源性释放可限制对重复运动的支气管收缩反应。我们研究的目的是确定吸入前列腺素（PG）E2是否能减轻哮喘患者运动诱发的支气管收缩或乙酰甲胆碱气道反应性。8名患有轻度稳定哮喘和运动性支气管收缩的受试者在4个不同的日子接受研究，间隔48小时。受试者在运动激发试验或乙酰甲胆碱激发试验前30分钟，以随机、交叉、双盲方式吸入PGE2或安慰剂。吸入PGE2可显著减轻运动性支气管收缩。安慰剂组运动后FEV1的平均最大下降百分比为26%（标准误3.7%），PGE2组为9.7%（标准误2.7%）（p<0.001）。PGE2还显著缩短了运动性支气管收缩的持续时间（p = 0.034）。然而，PGE2并未显著减轻乙酰甲胆碱气道反应性。安慰剂日导致FEV1下降20%的乙酰甲胆碱激发浓度几何平均值（PC20）为0.77（%标准误1.48），PGE2日后为1.41（%标准误2.20）（p = 0.30）。这些结果表明，吸入PGE2可显著减轻哮喘患者的运动性支气管收缩，并提示这种作用并非通过气道平滑肌的功能拮抗作用产生。
