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首页> 外文期刊>American Journal of Physiology >Effect of azelastine on platelet-activating factor-induced microvascular leakage in rat airways.
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Effect of azelastine on platelet-activating factor-induced microvascular leakage in rat airways.

机译：氮卓斯汀对血小板活化因子诱导的大鼠气道微血管渗漏的影响。

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摘要

To determine the effect of the antiallergic drug azelastine on airway mucosal inflammation, we studied airway microvascular permeability in response to platelet-activating factor (PAF) in pathogen-free rats. Vascular permeability and neutrophil accumulation were assessed by the percent area occupied by Monastral blue-labeled blood vessels and by myeloperoxidase-containing granulocytes, respectively, in whole mounts of the trachea and main bronchus. Intravenous PAF caused dose-dependent increases in the area density of Monastral blue-labeled vessels and neutrophil influx, and the former effect was inhibited by depletion of circulating neutrophils by cyclophosphamide or treatment with the neutrophil elastase inhibitor ONO-5046. Pretreatment with azelastine inhibited PAF-induced vascular leakage without affecting neutrophil accumulation. This inhibitory effect of azelastine was not seen in neutropenic rats and ONO-5046-treated rats. PAF increased neutrophil elastase contents in bronchoalveolar lavage fluid, an effect that was inhibited by azelastine. Therefore, azelastine attenuates PAF-induced airway mucosal microvascular leakage, probably involving inhibition of the release of neutrophil elastase from activated neutrophils.
机译：为了确定抗过敏药氮卓斯汀对气道粘膜炎症的影响，我们研究了无病原体大鼠中响应血小板活化因子（PAF）的气道微血管通透性。血管通透性和嗜中性粒细胞的积累分别通过气管和主支气管整个部位的Monastral蓝标血管和含髓过氧化物酶的粒细胞所占的面积百分比来评估。静脉内PAF引起剂量依赖性地增加了Monastral蓝色标记的血管和中性粒细胞流入的面积密度，并且前者的作用被环磷酰胺消耗循环中性粒细胞或中性粒细胞弹性蛋白酶抑制剂ONO-5046处理抑制。氮卓斯汀预处理可抑制PAF诱导的血管渗漏，而不会影响中性粒细胞的积累。氮卓斯汀的这种抑制作用在中性粒细胞减少的大鼠和ONO-5046处理的大鼠中未观察到。 PAF增加了支气管肺泡灌洗液中的中性粒细胞弹性蛋白酶含量，这被氮卓斯汀抑制。因此，氮卓斯汀减弱了PAF诱导的气道粘膜微血管渗漏，可能涉及抑制活化的中性粒细胞释放中性粒细胞弹性蛋白酶。

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