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前列环素对人吸入血小板活化因子诱导的支气管收缩和中性粒细胞减少的影响。

Effects of prostacyclin on bronchoconstriction and neutropenia induced by inhaled platelet-activating factor in man.

作者信息

Lammers J W, Kioumis I, McCusker M, Nichol G M, Barnes P J, Chung K F

机构信息

Department of Thoracic Medicine, Brompton Hospital, London, England.

出版信息

J Allergy Clin Immunol. 1990 Apr;85(4):763-9. doi: 10.1016/0091-6749(90)90196-b.

DOI:10.1016/0091-6749(90)90196-b
PMID:2109002
Abstract

We studied the effects of prostacyclin (PGI2) on the airway responses to platelet-activating factor (PAF) in a randomized and crossover study in eight normal subjects. PGI2 or diluent (glycine buffer) was continuously infused on 2 separate days. Two breaths of PAF (21 micrograms) were inhaled three times every 15 minutes and airflow at 30% of vital capacity from partial flow-volume curves (Vp30) was measured. PGI2 (4 ng/kg/min) had no effect on Vp30 or blood pressure, whereas heart rate increased from 70.3 +/- 3.9 to 73.7 +/- 4.0 beats/min (mean +/- SEM; p less than 0.01). Two subjects did not complete the study because of transient hypotension. PGI2 had no effect on PAF-induced bronchoconstriction with maximal decreases in Vp30 of 42.0 +/- 8.0% (p less than 0.01) during PGI2 and 49.8 +/- 14.2% (p less than 0.02) during diluent infusion. Ex vivo platelet aggregation to PAF (10(-9) to 10(-7) mol/L) was significantly inhibited by PGI2. Circulating neutrophils decreased from 4.7 +/- 0.9 x 10(9)/L to 1.5 +/- 0.3 x 10(9)/L (p less than 0.05) 5 minutes after the first PAF inhalation during diluent infusion, whereas there was no significant change with PGI2. Thus, PGI2 does not influence PAF-induced bronchoconstriction in man despite causing marked inhibition of ex vivo PAF-induced platelet aggregation and preventing the fall of neutrophils.

摘要

在一项针对8名正常受试者的随机交叉研究中,我们研究了前列环素(PGI2)对气道对血小板活化因子(PAF)反应的影响。在两个不同的日子里持续输注PGI2或稀释剂(甘氨酸缓冲液)。每隔15分钟吸入两次PAF(21微克),共三次,并根据部分流速-容量曲线(Vp30)测量肺活量30%时的气流。PGI2(4纳克/千克/分钟)对Vp30或血压无影响,而心率从70.3±3.9次/分钟增加到73.7±4.0次/分钟(平均值±标准误;p<0.01)。两名受试者因短暂性低血压未完成研究。PGI2对PAF诱导的支气管收缩无影响,在输注PGI2期间Vp30最大降低42.0±8.0%(p<0.01),在输注稀释剂期间为49.8±14.2%(p<0.02)。PGI2显著抑制了体外血小板对PAF(10^(-9)至10^(-7)摩尔/升)的聚集。在输注稀释剂期间,首次吸入PAF后5分钟,循环中性粒细胞从4.7±0.9×10^9/升降至1.5±0.3×10^9/升(p<0.05),而使用PGI2时无显著变化。因此,尽管PGI2能显著抑制体外PAF诱导的血小板聚集并防止中性粒细胞减少,但它并不影响人类体内PAF诱导的支气管收缩。

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Effects of prostacyclin on bronchoconstriction and neutropenia induced by inhaled platelet-activating factor in man.前列环素对人吸入血小板活化因子诱导的支气管收缩和中性粒细胞减少的影响。
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引用本文的文献

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Role for platelet-activating factor in asthma.血小板活化因子在哮喘中的作用。
Lipids. 1991 Dec;26(12):1277-9. doi: 10.1007/BF02536547.
2
Failure of salmeterol to inhibit circulating white cell responses and bronchoconstriction induced by platelet activating factor.沙美特罗未能抑制血小板活化因子诱导的循环白细胞反应和支气管收缩。
Thorax. 1992 Nov;47(11):948-51. doi: 10.1136/thx.47.11.948.