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吸入速尿对哮喘(特应性)受试者和(主动致敏)豚鼠抗原诱导的早期阻塞性反应的预防作用

Prevention of antigen-induced early obstructive reaction by inhaled furosemide in (atopic) subjects with asthma and (actively sensitized) guinea pigs.

作者信息

Robuschi M, Pieroni M, Refini M, Bianco S, Rossoni G, Magni F, Berti F

机构信息

Institute of Lung Diseases, University of Siena, Italy.

出版信息

J Allergy Clin Immunol. 1990 Jan;85(1 Pt 1):10-6. doi: 10.1016/0091-6749(90)90215-p.

DOI:10.1016/0091-6749(90)90215-p
PMID:2405040
Abstract

The present study was undertaken to determine the effect of furosemide on antigen-induced bronchoconstriction. Ten patients with stable asthma (eight men and two women), aged 17 to 48 years, were challenged with the same dose of allergen (Dermatophagoides pteronissinus, Parietaria, and grass mix) that had induced an FEV1 fall of at least 20% in a preliminary study on two occasions: immediately after placebo and furosemide (approximately 28 mg) administered by inhalation in random order and double-blind. Furosemide did not demonstrate any direct bronchodilator effect but markedly attenuated allergen-induced bronchoconstriction. The mean (95% confidence interval) maximum fall in FEV1 was 31.5% (40.2% to 22.8%) after placebo and 8.4% (11.8% to 4.9%) after furosemide administration. Furosemide, administered by aerosol to anesthetized guinea pigs actively sensitized to ovalbumin, dose dependently protected the animals from anaphylactic reaction. Infusion of furosemide (10 mg/kg for 10 minutes) failed to protect the animals from the anaphylactic response. In nonsensitized guinea pigs, the cardiovascular and pulmonary changes induced by histamine (10 micrograms/kg intravenously [i.v.]), leukotriene C4 (1 micrograms/kg i.v.), and platelet-activating factor (0.1 microgram/kg i.v.) were not modified by aerosol administration of furosemide (10 mg/ml for 10 minutes). In conclusion, inhaled furosemide induces a clear-cut protection against immediate obstructive reaction caused by areoallergerns and ovalbumin, both in subjects with asthma and actively sensitized guinea pigs, respectively.

摘要

本研究旨在确定呋塞米对抗原诱导的支气管收缩的影响。10例稳定期哮喘患者(8例男性,2例女性),年龄在17至48岁之间,接受了相同剂量的变应原(粉尘螨、墙草属和草混合物)激发试验,该变应原在初步研究中曾两次导致FEV1下降至少20%:在随机顺序双盲吸入安慰剂和呋塞米(约28mg)后立即进行。呋塞米未显示出任何直接的支气管扩张作用,但显著减轻了变应原诱导的支气管收缩。安慰剂后FEV1的平均(95%置信区间)最大下降为31.5%(40.2%至22.8%),呋塞米给药后为8.4%(11.8%至4.9%)。将呋塞米以气雾剂形式给予对卵清蛋白主动致敏的麻醉豚鼠,剂量依赖性地保护动物免受过敏反应。静脉输注呋塞米(10mg/kg,持续10分钟)未能保护动物免受过敏反应。在未致敏的豚鼠中,组胺(10μg/kg静脉注射)、白三烯C4(1μg/kg静脉注射)和血小板活化因子(0.1μg/kg静脉注射)诱导的心血管和肺部变化未因吸入呋塞米气雾剂(10mg/ml,持续10分钟)而改变。总之,吸入呋塞米分别在哮喘患者和主动致敏的豚鼠中,对气源性变应原和卵清蛋白引起的即刻阻塞性反应具有明确的保护作用。

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