Allen Gilman, Bates Jason H T
Department of Medicine, Vermont Lung Center, University of Vermont, Bulington, Vermont 05405-0075, USA.
J Appl Physiol (1985). 2004 Jan;96(1):293-300. doi: 10.1152/japplphysiol.00270.2003. Epub 2003 Aug 29.
In a previous study (Allen G, Lundblad LK, Parsons P, and Bates JH. J Appl Physiol 93: 1709-1715, 2002), our laboratory used deep inflations (DI) in mice to show that recruitment of closed lung units can be a very transient phenomenon in lung injury. The purpose of this study was to investigate how this transience of lung recruitment depends on the nature and degree of acute lung injury. Mice were administered 50 microl of either saline (n = 8), 0.01 M (n = 9) or 0.025 M (n = 8) hydrochloric acid, or 50 microg (n = 10) or 150 microg (n = 6) of LPS and were mechanically ventilated 24-48 h later. At various levels of positive end-expiratory pressure, two DIs were delivered, and forced oscillations were used to obtain a measure of lung stiffness (H) periodically over 7 min. After LPS exposure, pressure-volume curve hysteresis and recovery in H after DI were no different from saline-exposed controls despite 500 times more neutrophils in bronchoalveolar lavage fluid. Pressure-volume hysteresis and recovery in H were increased in acid-exposed mice (P < 0.001) and were correlated with bronchoalveolar lavage fluid protein content (R = 0.81). Positive end-expiratory pressure reduced recovery in H in all groups (P < 0.01) but reduced pressure-volume hysteresis in the acid-injured groups only (P < 0.001). We conclude that the effects of DIs in acute lung injury depend on the degree of lung injury but only to the extent that this injury reflects a disruption of the air-liquid interface.
在之前的一项研究中（艾伦·G、伦德布拉德·LK、帕森斯·P和贝茨·JH。《应用生理学杂志》93: 1709 - 1715，2002年），我们实验室在小鼠中使用深度充气（DI）来表明，在肺损伤中，闭合肺单位的募集可能是一种非常短暂的现象。本研究的目的是探讨肺募集的这种短暂性如何取决于急性肺损伤的性质和程度。给小鼠注射50微升生理盐水（n = 8）、0.01 M（n = 9）或0.025 M（n = 8）盐酸，或50微克（n = 10）或150微克（n = 6）脂多糖，24 - 48小时后进行机械通气。在不同水平的呼气末正压下，进行两次深度充气，并使用强迫振荡在7分钟内定期测量肺硬度（H）。脂多糖暴露后，尽管支气管肺泡灌洗液中的中性粒细胞比生理盐水暴露组多500倍，但压力 - 容积曲线滞后和深度充气后H的恢复与生理盐水暴露组无差异。酸暴露小鼠的压力 - 容积滞后和H的恢复增加（P < 0.001），且与支气管肺泡灌洗液蛋白含量相关（R = 0.81）。呼气末正压降低了所有组中H的恢复（P < 0.01），但仅降低了酸损伤组的压力 - 容积滞后（P < 0.001）。我们得出结论，深度充气在急性肺损伤中的作用取决于肺损伤的程度，但仅取决于这种损伤反映气液界面破坏的程度。
