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吸入性前列腺素E2对变应原诱导性哮喘的影响。

Effect of inhaled prostaglandin E2 on allergen-induced asthma.

作者信息

Pavord I D, Wong C S, Williams J, Tattersfield A E

机构信息

Respiratory Medicine Unit, City Hospital, Nottingham, England.

出版信息

Am Rev Respir Dis. 1993 Jul;148(1):87-90. doi: 10.1164/ajrccm/148.1.87.

DOI:10.1164/ajrccm/148.1.87
PMID:8317820
Abstract

Prostaglandin E2 (PGE2) is produced in the lung but unlike most other lipid mediators has potentially important antiallergic effects. Whether these properties are relevant to asthma has not been established. The effect of inhaled PGE2 on allergen-induced asthma was examined in a double-blind crossover study of eight subjects with asthma. In Study 1 subjects inhaled 100 micrograms PGE2 or placebo 5 min before a normal saline challenge, and FEV1 and bronchial reactivity to methacholine was measured at intervals for 7 h. In Study 2, which had a similar design, subjects inhaled the same dose of PGE2 or placebo followed by a dose of allergen previously shown to cause a fall in FEV1 of 20% or more. On the normal saline challenge day inhaled PGE2 caused a small increase in FEV1 that lasted for around 60 min; there was no difference in the provocative dose of methacholine causing a 20% fall in FEV1 (PD20) at 4 and 7 h compared with placebo. PGE2 caused marked inhibition of the early and late response to allergen. The mean maximum fall in FEV1 0 to 2 h after allergen was 37.8 and 7.7% with placebo and PGE2 pretreatment, respectively (mean difference 30%; 95% CI 15, 45%; p < 0.005). The mean maximum fall in FEV1 from 4 to 7 h after allergen was 25.5 and 8.8% respectively (mean difference 16.7%; 95% CI 4, 29%; p < 0.02). The methacholine PD20 fell significantly after allergen with placebo but not with PGE2. The difference was 1.5 doubling doses at both 4 and 7 h (p < 0.01 and p < 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

前列腺素E2(PGE2)在肺中产生,但与大多数其他脂质介质不同,它具有潜在的重要抗过敏作用。这些特性是否与哮喘相关尚未确定。在一项对8名哮喘患者的双盲交叉研究中,研究了吸入PGE2对变应原诱发哮喘的影响。在研究1中,受试者在生理盐水激发前5分钟吸入100微克PGE2或安慰剂,并在7小时内定期测量第一秒用力呼气容积(FEV1)和对乙酰甲胆碱的支气管反应性。在设计相似的研究2中,受试者吸入相同剂量的PGE2或安慰剂,随后吸入一剂先前已证明会导致FEV1下降20%或更多的变应原。在生理盐水激发日,吸入PGE2使FEV1有小幅增加,持续约60分钟;与安慰剂相比,在4小时和7小时时,导致FEV1下降20%的乙酰甲胆碱激发剂量(PD20)没有差异。PGE2对变应原的早期和晚期反应有显著抑制作用。变应原后0至2小时,安慰剂预处理组和PGE2预处理组FEV1的平均最大下降分别为37.8%和7.7%(平均差异30%;95%可信区间15,45%;p<0.005)。变应原后4至7小时,FEV1的平均最大下降分别为25.5%和8.8%(平均差异16.7%;95%可信区间4,29%;p<0.02)。变应原后,安慰剂组乙酰甲胆碱PD20显著下降,而PGE2组未下降。在4小时和7小时时差异均为1.5倍剂量(p<0.01和p<0.02)。(摘要截断于250字)

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