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前列腺素E_2和前列腺素F_(2α)正常就存在于人体的肺脏和支气管内。当发生过敏反应时,从豚鼠和大鼠的肺脏释放前列腺素F_(2α)(PGF_(2α)),在人类它可引起平滑肌收缩(在体内或在试管内)。哮喘患者对于吸入的PGF_(2α)有高度的敏感性,内生的PGF_(2α)可能对支气管哮喘的发作起着重要的作用。阿斯匹林和消炎痛能有效地抑制前列腺素的合成,因此有人认为阿斯匹林有支气管扩张的作用。但据报告有一组对阿斯匹林敏感者,在服阿斯匹林几分钟内,呼吸道阻塞的症状却加剧。为了确定对阿斯匹林敏感者哮喘的发作是否与前列腺素浓度的升高有关,作者测定了7例口服可溶性阿斯匹林诱发哮喘发作患者血浆PGE_2和PGF_(2α)的浓度。测定用力呼气时的肺活量(FVC)和1秒钟用力呼出量(FEV_1),同时测定最大呼吸容量(MBC)。这些肺
Prostaglandin E_2 and prostaglandin F_ (2α) are normally present in the lungs and bronchi of the human body. When allergic reactions occur, prostaglandin F_ (2α) (PGF_ (2α)) is released from the lungs of guinea pigs and rats, and in humans it causes smooth muscle contraction (in vivo or in vitro). Patients with asthma are highly sensitive to inhaled PGF 2α and endogenous PGF 2α may play an important role in the onset of bronchial asthma. Aspirin and indomethacin can effectively inhibit prostaglandin synthesis, so some people think that aspirin bronchodilation. However, a group of people who reported being aspirin-sensitive were reported to have symptoms of airway obstruction within minutes of serving aspirin. To determine if the onset of asthma in aspirin-susceptible subjects was associated with elevated prostaglandin levels, the authors measured plasma concentrations of PGE 2 and PGF 2α in seven patients with aspirin-induced asthma attacks. The vital capacity (FVC) and forced expiratory volume (FEV_1) at 1 second were measured during forced expiration and the maximum respiratory capacity (MBC) was measured at the same time. These lungs