研究人员Page关于β_2—兴奋剂抑制自然抗炎机制的假设是不完善的。肥大细胞释放各种炎症前介质,激活肥大细胞导致速发过敏反应及肺和皮肤的炎症。临床剂量的β_2—兴奋剂能抑制这些介质的释放以及其释放对哮喘病人产生的后果。人肺中的肥大细胞确能合成并贮存肝素蛋白多糖(主要目的是结合组织胺)但在肥大细胞IgE介导的激活后的释放不到 Researchers Page’s hypothesis that β_2-stimulants suppress natural anti-inflammatory mechanisms is imperfect. Mast cells release a variety of pre-inflammatory mediators, activating mast cells leading to immediate hypersensitivity reactions and inflammation of the lungs and skin. The clinical dose of β_2-agonists inhibits the release of these agents and the consequences of their release on asthmatic patients. Mast cells in the human lung can indeed synthesize and store heparin proteoglycans (the primary purpose is to bind to histamine) but not to IgE-mediated activation of mast cells