Nizankowska E, Michalska Z, Wandzilak M, Radomski M, Marcinkiewicz E, Gryglewski R J, Szczeklik A
Department of Medicine, Copernicus Academy of Medicine, Cracow, Poland.
Eicosanoids. 1988;1(1):45-8.
Aspirin (ASA)-induced asthma is a distinct clinical syndrome in which bronchoconstrictive response to nonsteroidal anti-inflammatory drugs can be predicted on the basis of their in vitro activity as inhibitors of cyclooxygenase. In ten ASA-sensitive asthmatics and ten matched healthy controls we measured 12-hydroxy-eicosatetraenoic acid (12-HETE) production by platelets and 5-hydroxy-eicosatetraenoic acid (5-HETE) and leukotriene B4 (LTB4) production by polymorphonuclear leucocytes. The blood cells were obtained before administration of the threshold doses of ASA and during the ASA-induced reactions. Initial levels of eicosanoids determined did not differ between the two groups. In both groups, after ASA challenge, 12-HETE rose to similar levels while 5-HETE and LTB4 remained unchanged. These data do not support the concept that an abnormality in the regulation of arachidonic acid oxidative pathways in ASA-sensitive asthmatics is a generalized phenomenon which embraces the platelets and leucocytes; rather it is inhibition of cyclo-oxygenase within the tissues of the respiratory tract that triggers asthmatic attacks in the sensitive patients.
阿司匹林（ASA）诱发的哮喘是一种独特的临床综合征，其中对非甾体抗炎药的支气管收缩反应可根据其作为环氧化酶抑制剂的体外活性来预测。我们在10名对ASA敏感的哮喘患者和10名匹配的健康对照者中，测量了血小板产生12-羟基-二十碳四烯酸（12-HETE）的情况，以及多形核白细胞产生5-羟基-二十碳四烯酸（5-HETE）和白三烯B4（LTB4）的情况。血细胞在给予ASA阈值剂量之前以及在ASA诱发反应期间获取。两组中所测定的类花生酸初始水平并无差异。在两组中，ASA激发后，12-HETE升至相似水平，而5-HETE和LTB4保持不变。这些数据不支持以下概念，即对ASA敏感的哮喘患者中花生四烯酸氧化途径调节异常是一种涉及血小板和白细胞的普遍现象；相反，是呼吸道组织中环氧化酶的抑制引发了敏感患者的哮喘发作。
