Mai X-M, Böttcher M F, Bruhammar M, Nilsson L, Zetterström O
Department of Molecular and Clinical Medicine, Division of Pediatrics, Linköping University, Linköping, Sweden.
Allergy. 2005 Jan;60(1):60-4. doi: 10.1111/j.1398-9995.2004.00623.x.
The inflammatory mechanisms of hypertonic saline-induced bronchoconstriction are not well understood.
Seventeen asthmatics with (n=11) and without bronchial hyperresponsiveness (BHR) (n=6) and 18 randomly selected nonatopic nonasthmatic controls without BHR were evaluated by urine samples collected before and 1 h after hypertonic saline provocation test. Histamine, 11beta-PGF2alpha, and LTE4 were analysed by enzyme immunoassay (EIA) and eosinophil protein X (EPX) by radioimmunoassay (RIA).
The levels of leukotriene E4 (LTE4) increased significantly after the challenge tests, both in the asthmatics (median: 354 pg/mg pre-challenge vs. 628 pg/mg post-challenge; P=0.05) and in the controls (median: 294 pg/mg pre-challenge vs. 460 pg/mg post-challenge; P <0.01). The levels of histamine also increased significantly in the latter (median: 299 micromol/mg pre-challenge vs. 569 micromol/mg post-challenge; P=0.03). However, the levels of 11beta-PGF2alpha and EPX did not change significantly after the challenge tests either in the asthmatics or in the controls.
The inhalation of hypertonic saline increased urinary excretion of LTE4 both in the asthmatics and in the controls. The slight increase of leukotrienes was enough to induce airway obstruction in some of the asthmatics, because of the hyperresponsiveness in their airways.
高渗盐水诱导支气管收缩的炎症机制尚未完全明确。
对17例哮喘患者(其中11例有支气管高反应性[BHR],6例无BHR)和18例随机选取的无BHR的非特应性非哮喘对照者,在高渗盐水激发试验前及激发后1小时采集尿液样本进行评估。采用酶免疫测定法(EIA)分析组胺、11β - PGF2α和白三烯E4(LTE4),采用放射免疫测定法(RIA)分析嗜酸性粒细胞蛋白X(EPX)。
激发试验后,哮喘患者(中位数:激发前354 pg/mg,激发后628 pg/mg;P = 0.05)和对照者(中位数:激发前294 pg/mg,激发后460 pg/mg;P <0.01)的白三烯E4(LTE4)水平均显著升高。对照者的组胺水平也显著升高(中位数:激发前299 μmol/mg,激发后569 μmol/mg;P = 0.03)。然而,激发试验后,哮喘患者和对照者的11β - PGF2α和EPX水平均无显著变化。
吸入高渗盐水可使哮喘患者和对照者的尿液中LTE4排泄增加。白三烯的轻微增加足以在一些哮喘患者中诱发气道阻塞,因为他们的气道具有高反应性。