应激性肺毛细血管损伤。

J B West, O Mathieu-Costello
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引用次数: 0

摘要

肺特别容易受伤,因为血气屏障非常薄。此外,当毛细血管压力升高或肺膨胀到很大体积时,屏障中的机械应力变得非常高。薄侧血气屏障的强度可归因于基底膜中的IV型胶原蛋白。肺毛细血管壁的异常高应力导致超微结构改变,包括肺泡上皮和毛细血管内皮层的破坏。所有的纯种马在奔跑时都会折断肺毛细血管。此外,优秀的人类运动员在高水平的运动中会发生血气屏障渗透性的变化。导致应激衰竭的病理情况包括:1)高原肺水肿;2)神经源性肺水肿;3)严重的左心室衰竭;4)二尖瓣狭窄;5)肺部过度膨胀。随着毛细血管压力的升高,出现从低渗透性到高渗透性水肿的频谱。肺动脉毛细血管重构明显发生在高毛细血管压力下。很可能毛细血管的细胞外基质在响应毛细血管壁应力时受到持续调节。
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Stress-induced injury of pulmonary capillaries.

The lung is particularly vulnerable to injury because the blood-gas barrier is so extremely thin. Furthermore, the mechanical stresses in the barrier become very high when capillary pressure is raised, or when the lung is inflated to a high volume. The strength of the blood-gas barrier on the thin side can be attributed to the type IV collagen in the basement membranes. Abnormally high stresses in the walls of the pulmonary capillaries result in ultrastructural changes including disruptions of both the alveolar epithelial and capillary endothelial layers. All Thoroughbred racehorses break their pulmonary capillaries when they gallop. Also, elite human athletes develop changes in the permeability of the blood-gas barrier at high levels of exercise. Pathological conditions resulting in stress failure include: 1) high-altitude pulmonary edema; 2) neurogenic pulmonary edema; 3) severe left ventricular failure; 4) mitral stenosis; and 5) overinflation of the lung. There is a spectrum of low permeability to high permeability edema as the capillary pressure is raised. Remodeling of pulmonary capillaries apparently occurs at high capillary pressures. It is likely that the extracellular matrix of the capillaries is continuously regulated in response to capillary wall stress.

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