Tsuda A, Otani Y, Butler J P
Physiology Program, Harvard School of Public Health, Boston, Massachusetts 02115, USA.
J Appl Physiol (1985). 1999 Mar;86(3):977-84. doi: 10.1152/jappl.1999.86.3.977.
Mixing associated with "stretch-and-fold" convective flow patterns has recently been demonstrated to play a potentially important role in aerosol transport and deposition deep in the lung (J. P. Butler and A. Tsuda. J. Appl. Physiol. 83: 800-809, 1997), but the origin of this potent mechanism is not well characterized. In this study we hypothesized that even a small degree of asynchrony in otherwise reversible alveolar wall motion is sufficient to cause flow irreversibility and stretch-and-fold convective mixing. We tested this hypothesis using a large-scale acinar model consisting of a T-shaped junction of three short, straight, square ducts. The model was filled with silicone oil, and alveolar wall motion was simulated by pistons in two of the ducts. The pistons were driven to generate a low-Reynolds-number cyclic flow with a small amount of asynchrony in boundary motion adjusted to match the degree of geometric (as distinguished from pressure-volume) hysteresis found in rabbit lungs (H. Miki, J. P. Butler, R. A. Rogers, and J. Lehr. J. Appl. Physiol. 75: 1630-1636, 1993). Tracer dye was introduced into the system, and its motion was monitored. The results showed that even a slight asynchrony in boundary motion leads to flow irreversibility with complicated swirling tracer patterns. Importantly, the kinematic irreversibility resulted in stretching of the tracer with narrowing of the separation between adjacent tracer lines, and when the cycle-by-cycle narrowing of lateral distance reached the slowly growing diffusion distance of the tracer, mixing abruptly took place. This coupling of evolving convective flow patterns with diffusion is the essence of the stretch-and-fold mechanism. We conclude that even a small degree of boundary asynchrony can give rise to stretch-and-fold convective mixing, thereby leading to transport and deposition of fine and ultrafine aerosol particles deep in the lung.
最近已证明,与“拉伸-折叠”对流流动模式相关的混合在肺部深处的气溶胶传输和沉积中可能发挥重要作用(J.P. 巴特勒和A. 津田。《应用生理学杂志》83: 800 - 809, 1997),但这种强大机制的起源尚未得到很好的表征。在本研究中,我们假设,即使在原本可逆的肺泡壁运动中存在很小程度的不同步,也足以导致流动不可逆以及拉伸-折叠对流混合。我们使用一个由三条短直方形管道的T形连接处组成的大型腺泡模型来检验这一假设。模型中充满硅油,通过其中两条管道中的活塞模拟肺泡壁运动。驱动活塞以产生低雷诺数循环流,边界运动中有少量不同步,其调整程度与在兔肺中发现的几何(与压力-容积相对)滞后程度相匹配(H. 三木、J.P. 巴特勒、R.A. 罗杰斯和J. 莱尔。《应用生理学杂志》75: 1630 - 1636, 1993)。将示踪染料引入系统并监测其运动。结果表明,即使边界运动中存在轻微不同步也会导致流动不可逆,并伴有复杂的示踪剂漩涡图案。重要的是,运动不可逆导致示踪剂拉伸,相邻示踪剂线之间的间距变窄,当横向距离逐周期变窄达到示踪剂缓慢增长的扩散距离时,混合突然发生。这种不断演变的对流流动模式与扩散的耦合是拉伸-折叠机制的本质。我们得出结论,即使是很小程度的边界不同步也会引起拉伸-折叠对流混合,从而导致细颗粒和超细气溶胶颗粒在肺部深处的传输和沉积。