Deal E C, Wasserman S I, Soter N A, Ingram R H, McFadden E R
J Clin Invest. 1980 Mar;65(3):659-65. doi: 10.1172/JCI109711.
To determine whether mediators of immediate hypersensitivity played a role in the pathogenesis of exercise-induced asthma, we measured the concentration of histamine and neutrophil-chemotactic activity present in systemic arterial blood during thermal challenges in five asymptomatic asthmatics. Because exercise-induced asthma has been shown to be a result of respiratory heat loss and because respiratory heat loss during isocapnic hyperventilation has been shown to give identical responses, we chose the latter provocational method in order to minimize increases in cardiac output that might interfere with the interpretation of mediator concentrations in arterial blood. Multiple aspects of pulmonary mechanics were also recorded before and after provocation. The results of these studies were then compared with the effects observed when the same subjects inhaled aerosols of specific antigens on the same day. Each challenge produced identical alterations in lung function, and neither was associated with consistent changes in arterial histamine. However, antigen provocation evoked a sustained and prolonged release of neutrophil chemotactic activity in each subject, whereas isocapnic hyperventilation with cold air was without effect. These data strongly suggest that mast-cell derived mediators are not involved in the development or maintenance of the bronchial obstruction that follows exercise in asthmatics.
为了确定速发型超敏反应介质在运动诱发哮喘的发病机制中是否起作用，我们在5名无症状哮喘患者进行热刺激期间，测量了体循环动脉血中组胺的浓度和中性粒细胞趋化活性。由于运动诱发哮喘已被证明是呼吸热损失的结果，并且由于等碳酸过度通气期间的呼吸热损失已被证明会产生相同的反应，我们选择了后一种激发方法，以尽量减少可能干扰动脉血中介质浓度解释的心输出量增加。在激发前后还记录了肺力学的多个方面。然后将这些研究结果与同一天相同受试者吸入特异性抗原气雾剂时观察到的效应进行比较。每次激发都会引起肺功能相同的改变，并且两者均与动脉组胺的持续变化无关。然而，抗原激发在每个受试者中引起中性粒细胞趋化活性的持续和延长释放，而冷空气等碳酸过度通气则没有效果。这些数据强烈表明，肥大细胞衍生的介质不参与哮喘患者运动后支气管阻塞的发生或维持。
