Hirsch J A, Tokayer J L, Robinson M J, Sackner M A
J Appl Physiol. 1975 Aug;39(2):242-6. doi: 10.1152/jappl.1975.39.2.242.
The impairment of mucociliary transport by dry air breathing and the restoration of function with subsequent humidification of inspired air were investigated in anesthetized dogs. Tracheal mucous velocity was measured by a cinebronchofiberscopic technique. The breathing of dry air through an uncuffed endotracheal tube produced almost complete cessation of the flow of tracheal mucus after 3 h. Subsequent breathing of air at 38 degrees C with 100% relative humidity restored tracheal mucous velocity to control values by the end of and additional 3 h. Histologic examination of the trachea at the end of the 3-h dry air breathing period revealed focal areas of sloughing of the ciliated epithelium and submucosal inflammation. Although morphometry was not employed, the inflammatory changes appeared to have progressed during 3 h of breathing fully humidified air subsequent to the dry air breathing period. These findings were consistent with previous reports that the inflammatory response to injury of the tracheobronchial mucosa might be delayed and that the mucociliary transport system has a great deal of functional reserve. We found that an artificial heat and moisture exchanger placed on the proximal end of an endotracheal tube partially protects against the suppression of tracheal mucous velocity caused by dry air breathing.
在麻醉犬身上研究了通过呼吸干燥空气对黏液纤毛运输的损害以及随后通过对吸入空气进行加湿来恢复功能的情况。采用纤维支气管镜电影摄影技术测量气管黏液速度。通过无套囊气管内导管呼吸干燥空气3小时后，气管黏液流动几乎完全停止。随后呼吸38摄氏度、相对湿度100%的空气，在额外的3小时结束时，气管黏液速度恢复到对照值。在呼吸干燥空气3小时结束时对气管进行组织学检查，发现有纤毛上皮脱落和黏膜下炎症的局灶性区域。尽管未采用形态计量学方法，但在干燥空气呼吸期之后呼吸完全湿润空气的3小时内，炎症变化似乎有所进展。这些发现与先前的报告一致，即气管支气管黏膜损伤的炎症反应可能会延迟，并且黏液纤毛运输系统具有大量的功能储备。我们发现，放置在气管内导管近端的人工热湿交换器可部分防止因呼吸干燥空气而导致的气管黏液速度抑制。
