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吸入倍氯米松对致敏受试者中甲苯二异氰酸酯诱导的迟发性哮喘反应及对乙酰甲胆碱反应性增加的剂量依赖性抑制作用。

Dose-dependent inhibitory effect of inhaled beclomethasone on late asthmatic reactions and increased responsiveness to methacholine induced by toluene diisocyanate in sensitised subjects.

作者信息

De Marzo N, Fabbri L M, Crescioli S, Plebani M, Testi R, Mapp C E

机构信息

Institute of Occupational Medicine, University of Padova, Italy.

出版信息

Pulm Pharmacol. 1988;1(1):15-20. doi: 10.1016/0952-0600(88)90005-1.

Abstract

To determine whether inhaled beclomethasone, both at low and at high doses, inhibits late asthmatic reactions and the associated increase in airway responsiveness induced by toluene diisocyanate (TDI), we studied 9 sensitised subjects. Low dose beclomethasone (200 micrograms bid), high dose beclomethasone aerosol (1000 micrograms bid), and placebo were administered for 7 days before TDI inhalation challenge to each subject, according to a double-blind, crossover study design. The washout period between the treatments was at least 1 week. When the subjects were treated with placebo, forced expiratory volume in 1 sec (FEV1) markedly decreased after exposure to TDI. By contrast, high dose beclomethasone prevented the late asthmatic reaction and the low dose partially inhibited the reaction. With placebo the mean (+/- SE) value of FEV1 4 h after exposure to TDI was 2.6 +/- 0.17 L, which went to 3.3 +/- 0.12 after low dose beclomethasone, and to 3.5 +/- 0.15 L after high dose of beclomethasone (significant difference in the decrease of FEV1 in the 8 h after exposure to TDI, between treatments: F = 9.87, (P less than 0.001), After treatment with placebo or with low dose beclomethasone, airway responsiveness to methacholine increased 8 h after exposure to TDI. With placebo, the PD20 decreased from 0.66 mg (Geometric Standard Error of the Mean [GSEM], 1.38) to 0.18 mg (GSEM, 1.46); with low dose inhaled beclomethasone, the PD20 decreased from 0.93 mg (GSEM, 1.42) to 0.36 mg (GSEM, 1.63).(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

为了确定低剂量和高剂量吸入倍氯米松是否能抑制迟发性哮喘反应以及由甲苯二异氰酸酯(TDI)诱发的气道反应性相关增加,我们研究了9名致敏受试者。根据双盲、交叉研究设计,在对每位受试者进行TDI吸入激发试验前7天,给予低剂量倍氯米松(200微克,每日两次)、高剂量倍氯米松气雾剂(1000微克,每日两次)和安慰剂。治疗之间的洗脱期至少为1周。当受试者接受安慰剂治疗时,暴露于TDI后1秒用力呼气量(FEV1)显著下降。相比之下,高剂量倍氯米松可预防迟发性哮喘反应,低剂量部分抑制该反应。使用安慰剂时,暴露于TDI后4小时FEV1的平均(±标准误)值为2.6±0.17升,低剂量倍氯米松治疗后升至3.3±0.12升,高剂量倍氯米松治疗后升至3.5±0.15升(治疗之间,暴露于TDI后8小时FEV1下降的显著差异:F = 9.87,(P<0.001))。在接受安慰剂或低剂量倍氯米松治疗后,暴露于TDI后8小时气道对乙酰甲胆碱的反应性增加。使用安慰剂时,PD20从0.66毫克(几何平均标准误[GSEM],1.38)降至0.18毫克(GSEM,1.46);使用低剂量吸入倍氯米松时,PD20从0.93毫克(GSEM,1.42)降至0.36毫克(GSEM,1.63)。(摘要截断于250字)

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