On the role of surface tension in the pathophysiology of emphysema
On the role of surface tension in the pathophysiology of emphysema
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DOI：
10.1164/rccm.200406-770pp
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发表时间：
2005-02-15
影响因子：
24.7
通讯作者：
Suki, B
中科院分区：
文献类型：
--
作者：
Ingenito, EP;Tsai, LW;Suki, B
肺气肿是一种以肺实质破坏为特征的疾病，如果没有定义的话。这种破坏被认为主要是由于肺泡室内产生的蛋白水解酶和自由基对有害刺激的破坏作用。其他因素，包括上皮细胞和内皮细胞的凋亡，对组织损伤的不完全肺重塑，以及机械力，也可能起到作用(2，3)。随着时间的推移，实质的破坏和不完全的愈合会导致组织胶原和弹性蛋白的丢失，肺泡空隙的扩大，最终导致晚期肺气肿的典型生理特征：过度充盈，在给定的肺容量下失去弹性反冲，失去气体交换的表面积，以及严重的气流限制。由于正常肺和肺气肿肺的主要组织学差异是肺实质的丢失，因此得出肺气肿的生理学是由反冲组织成分的丢失所决定的结论是合乎逻辑的。然而，在正常肺中，在液体充盈状态下，反冲压力降低50%到60%，这表明在任何给定的压力(4，5)下，表面张力对肺反冲有很大的贡献。一个明显的问题是，肺气肿是否也是如此。虽然肺气肿主要不是表面活性物质的紊乱，但对正常肺表面张力的关键作用的反应表明，表面张力和表面活性物质单层对整个肺反冲的生理效应在肺气肿肺中一定会发生改变。否则，人们可能会天真地认为肺气肿的后座力永远不会降到正常水平的一半到三分之二以下。为什么要问这个问题？肺气肿是对肺组织的不可逆转的破坏。表面张力对反冲的贡献是30%、50%还是70%，或者这一百分比是否随着疾病的进展而变化，这真的重要吗？出于后面概述的原因，我们相信答案是响亮的“是的”。如果表面张力确实起到了重要作用，设计用于安全和有利地调节表面张力的表面活性物质可能被用来增加肺气肿的反冲。
Pulmonary emphysema is a disease that is characterized, if not defined, by the destruction of lung parenchyma (1). This destruction is believed to result principally from the damaging effects of proteolytic enzymes and free radicals generated within the alveolar compartment in response to noxious stimuli. Other factors, including epithelial and endothelial cell apoptosis, incomplete lung remodeling in response to tissue injury, and mechanical forces, may also contribute (2, 3). Over many years, parenchymal destruction and incomplete healing result in loss of tissue collagen and elastin, enlargement of alveolar airspaces, and, ultimately, the classic physiologic characteristics of advanced emphysema: hyperinffation, loss of elastic recoil at a given lung volume, loss of surface area for gas exchange, and severe ffow limitation. Because the major histologic difference between the normal lung and the emphysema lung is loss of lung parenchyma, it is logical to conclude that the physiology of emphysema is mechanically determined by loss of the tissue component of recoil. However, in the normal lung, recoil pressure decreases by 50 to 60% in the ffuid-filled state, indicating that surface tension contributes substantially to lung recoil at any given pressure (4, 5). An obvious question is whether the same is true in the emphysema lung. Although emphysema is not primarily a disorder of surfactant, reffection on the critical role of surface tension in the normal lung indicates that an alteration in the physiologic effects of surface tension and the surfactant monolayer on overall lung recoil must occur in the emphysema lung. Otherwise one might naively expect that recoil pressure in emphysema could never decrease below one half to two thirds of normal. Why ask this question? Emphysema is irreversible destruction of lung tissue. Does it really matter whether surface tension contributes 30, 50, or 70% of recoil, or whether this percentage changes as disease progresses? For reasons outlined later, we believe the answer is a resounding “yes.” If surface tension does contribute significantly, surface-active agents designed to safely and favorably modulate surface tension might be used to increase recoil in emphysema.