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人类屏气潜水时气道和肺泡塌陷的力学原理。

Mechanics of airway and alveolar collapse in human breath-hold diving.

作者信息

Fitz-Clarke John R

机构信息

Department of Physiology and Biophysics, Dalhousie University, 5849 University Avenue, Halifax, NS, Canada B3H 4H7.

出版信息

Respir Physiol Neurobiol. 2007 Nov 15;159(2):202-10. doi: 10.1016/j.resp.2007.07.006. Epub 2007 Jul 27.

Abstract

A computational model of the human respiratory tract was developed to study airway and alveolar compression and re-expansion during deep breath-hold dives. The model incorporates the chest wall, supraglottic airway, trachea, branched airway tree, and elastic alveoli assigned time-dependent surfactant properties. Total lung collapse with degassing of all alveoli is predicted to occur around 235 m, much deeper than estimates for aquatic mammals. Hysteresis of the pressure-volume loop increases with maximum diving depth due to progressive alveolar collapse. Reopening of alveoli occurs stochastically as airway pressure overcomes adhesive and compressive forces on ascent. Surface area for gas exchange vanishes at collapse depth, implying that the risk of decompression sickness should reach a plateau beyond this depth. Pulmonary capillary transmural stresses cannot increase after local alveolar collapse. Consolidation of lung parenchyma might provide protection from capillary injury or leakage caused by vascular engorgement due to outward chest wall recoil at extreme depths.

摘要

为了研究深度屏气潜水过程中气道和肺泡的压缩与再扩张,开发了一种人体呼吸道的计算模型。该模型纳入了胸壁、声门上气道、气管、分支气道树以及具有时间依赖性表面活性物质特性的弹性肺泡。预计所有肺泡排气后全肺塌陷会在约235米处发生,比水生哺乳动物的估计深度要深得多。由于肺泡逐渐塌陷,压力-容积环的滞后现象随着最大潜水深度的增加而增大。随着气道压力在上升过程中克服黏附力和压缩力,肺泡随机重新开放。气体交换表面积在塌陷深度消失,这意味着减压病的风险在超过此深度后应趋于平稳。局部肺泡塌陷后肺毛细血管跨壁应力无法增加。肺实质的实变可能会保护肺部免受极端深度时胸壁向外反冲导致的血管充血引起的毛细血管损伤或渗漏。

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