Kotaru Chakradhar, Hejal Rana B, Finigan J H, Coreno Albert J, Skowronski Mary E, Brianas Lori, McFadden E R
General Clinical Research Center of Case Western Reserve University School of Medicine and Division of Pulmonary and Critical Care Medicine and Department of Medicine of University Hospitals of Cleveland, OH 44106, USA.
J Appl Physiol (1985). 2003 Jan;94(1):227-33. doi: 10.1152/japplphysiol.00551.2002. Epub 2002 Sep 13.
To determine whether drying and hypertonicity of the airway surface fluid (ASF) are involved in thermally induced asthma, nine subjects performed isocapnic hyperventilation (HV) (minute ventilation 62.2 +/- 8.3 l/min) of frigid air (-8.9 +/- 3.3 degrees C) while periciliary fluid was collected endoscopically from the trachea. Osmolality was measured by freezing-point depression. The baseline 1-s forced expiratory volume was 73 +/- 4% of predicted and fell 26.4% 10 min postchallenge (P > 0.0001). The volume of ASF collected was 11.0 +/- 2.2 microl at rest and remained constant during and after HV as the airways narrowed (HV 10.6 +/- 1.9, recovery 6.5 +/- 1.7 microl; P = 0.18). The osmolality also remained stable throughout (rest 336 +/- 16, HV 339 +/- 16, and recovery 352 +/- 19 mosmol/kgH(2)O, P = 0.76). These data demonstrate that airway desiccation and hypertonicity of the ASF do not develop during hyperpnea in asthma; therefore, other mechanisms must cause exercise- and hyperventilation-induced airflow limitation.
为了确定气道表面液体(ASF)的干燥和高渗是否与热诱导哮喘有关,九名受试者对冷空气(-8.9±3.3℃)进行了等碳酸通气(HV)(分钟通气量62.2±8.3升/分钟),同时通过内镜从气管收集纤毛周液体。通过冰点降低法测量渗透压。基线1秒用力呼气量为预测值的73±4%,激发后10分钟下降了26.4%(P>0.0001)。静息时收集的ASF体积为11.0±2.2微升,在HV期间和之后随着气道变窄保持恒定(HV时为10.6±1.9微升,恢复时为6.5±1.7微升;P=0.18)。渗透压在整个过程中也保持稳定(静息时为336±16,HV时为339±16,恢复时为352±19毫摩尔/千克H₂O,P=0.76)。这些数据表明,哮喘患者在深呼吸期间不会出现气道干燥和ASF高渗;因此,其他机制必定导致运动和通气诱导的气流受限。