ASPIRIN-EVOKED SYNDROMES--SYSTEMATIC MAST CELL ACTIVATION AND ASTHMA

这项研究针对触发的两种临床症状 通过摄入阿司匹林和其他环氧合酶抑制剂。 阿司匹林诱发哮喘(AEM)与支气管痉挛有关，通常 严重，而阿司匹林诱导的系统性肥大细胞激活(AEM) 会导致脸色发红，有时还会出现低血压， 肥大细胞介体系统性释放的其他后果。 对AEM的拟议研究将描述调解人的特征 局部挑战后释放到支气管肺泡腔 用阿司匹林。大鼠的生化和组织学反应 将评估上呼吸道对环氧合酶的抑制作用，并 环氧合酶产物抑制的假说 AEM患者的支气管收缩将被选择性地 测试过。 在-AEM患者中，初步观察到小剂量 阿司匹林实际上增加了肥大细胞介质的释放， PGD2，将在进一步的研究中进行检测。问题是，是否 前列腺素E_2或血栓素A_2是环氧合酶产物 将检查抑制肥大细胞介体释放，以及 环氧合酶抑制对细胞形态的影响 皮肤肥大细胞及其与其他细胞的相互作用。 生化、组织学和组织化学的综合评价 这两个综合征对阿司匹林的功能性反应应该 为他们的病理生理学提供了新的见解。

This research addresses two clinical syndromes that are triggered by the ingestion of aspirin and other cyclooxygenase inhibitors. Aspirin-evoked asthma (AEM) is associated with bronchospasm, often severe, whereas aspirin-evoked systemic mastocyte activation (AEM) produces a syndrome of flushing, occasionally hypotension, and other consequences of the systemic release of mast cell mediators. The proposed studies on AEM will characterize the mediators released into the bronchoalveolar space following local challenge with aspirin. The biochemical and histologic responses of the upper airway to cyclooxygenase inhibition will be evaluated, and the hypothesis that a cyclooxygenase product restrains bronchoconstriction in patients with AEM will be selectively tested. In patients with-AEM, the preliminary observation that low doses of aspirin actually increase the release of the mast cell mediator, PGD2, will be examined in further studies. The question of whether either PGE2 or thromboxane A2 are the cyclooxygenase products that restrain mast cell mediator release will be examined, as will the consequences of cyclooxygenase inhibition on the morphology of cutaneous mast cells and their interactions with other cells. Integrated assessment of the biochemical, histological and functional response to aspirin in these two syndromes should provide new insights into their pathophysiology.