运动性哮喘的发病机制是紧密相连的热量和水通量开发大量的支气管树在空调内的空气。本事件都与呼吸热量交换的过程。有一些争议,最近的证据显示有气道温度下降在快速呼吸,其次是快速加热时通风减少。高通风,结合低温移动空气将从上到下呼吸道调节过程。多运动需要热量和水的粘膜将完全饱和的吸气体温(1991欧元和J)。数量越大的热能转移,航空公司将成为冷却器,他们re-warm越迅速,越来越多的支气管缩小(1991欧元和J)。另一方面,低通风或高湿度的空气吸入这些交流减少,所以限制热变化,导致气道阻塞的发展。支气管缩小将改变严重,如果任何组件cooling-rewarming周期的增加或扩大(中国投资1992)。相同的胸内的热剖面和气流限制都是由运动和换气过度。它并不完全清楚intra-airway热通量产生支气管缩小。快速的呼吸可能会导致粘膜表面水的蒸发和渗透性的增加,导致细胞脱粒和气道平滑肌的收缩(和牧师说1985)。不过,没有任何证据表明气道枯竭。另一种理论表明运动性哮喘结果从微循环在气道壁充血水肿的形成,不得涉及支气管平滑肌的收缩。航空公司与哮喘病人遭受有hyperplasic毛细血管床(J分册1960)比正常人更多的渗透。血管的收缩和扩张导致每个气道的冷却和加热,与肺功能的变化(中国投资1992)。
澳洲护理学论文代写：运动性哮喘
The pathogenesis of exercise-induced asthma is closely connected with the fluxes in heat and water that develop inside the tracheobronchial tree during the conditioning of large volumes of air. The proceeding events are linked to the process of respiratory heat exchange. There has been some controversy, the bulk of recent evidence shows there is a fall in airway temperature during rapid breathing, followed by rapid reheating when ventilation decreases. High ventilation, in combination with a low temperature of moved air pushes the conditioning process from the upper to the lower airway. Much movement of heat and water from the mucosa is needed to bring the inspired air to full saturation at body temperature (Eur Respir J 1991). The larger the quantity of thermal energy that is transferred, the cooler the airways will become, the more rapidly they re-warm, and the more the bronchi are narrowed (Eur Respir J 1991). On the other hand, low ventilation or the inhalation of air with high humidity decreases these exchanges, so limiting the thermal changes that lead to the development of airway obstruction. The bronchial narrowing will change severely, if any component of the cooling-rewarming cycle is increased or enlarged (J Clin Invest 1992). The same intrathoracic thermal profile and airflow limitation are both produced by exercise and hyperventilation. It is not fully clear how intra-airway thermal fluxes produce bronchial narrowing. Rapid breathing may cause the evaporation of mucosal surface water and an increase in osmolarity, resulting in post-cell degranulation and constriction of airway smooth muscles (Rev Respir Dis 1985). Still, there is not any evidence that airway dries up. Another theory states that exercise-induced asthma results from hyperemia of the microcirculation in the airway wall with the formation of edema and may not involve constriction of the bronchial smooth muscle. The airways in patients that suffer with asthma have a hyperplasic capillary bed (J Clin Pathol 1960) that is more permeable than in normal people. The constriction and dilatation of the vessels causes the cooling and heating of each airway, with changes in the pulmonary function (J Clin Invest 1992).
