Barnas G M, Sprung J, Kahn R, Delaney P A, Agarwal M
Department of Anesthesiology, University of Maryland, Baltimore 21201, USA.
J Appl Physiol (1985). 1995 May;78(5):1889-97. doi: 10.1152/jappl.1995.78.5.1889.
How pulmonary edema affects lung tissue and airway properties is not clear. From measurements of airway pressure and flow, we measured lung elastance (EL) and resistance (RL) in 5 anesthetized-paralyzed open-chested dogs during sinusoidal forcing in the frequency (f) and tidal volume (VT) ranges of normal breathing. RL was divided into its tissue (Rti) and airway (Raw) components from measurements of alveolar pressure through capsules glued to the lung surface. After induction of severe pulmonary edema by injection of oleic acid into the right atrium, forcing was repeated at the same mean airway pressure (Paw) as in control animals (11 cmH2O) and at a higher Paw (14 cmH2O), as would occur in closed-chested dogs during edema (G. M. Barnas, D. Stamenovic, and K. R. Lutchen. J. Appl. Physiol. 73: 1040-1046, 1992). Edema increased EL, and this increase was greater at Paw = 14 cmH2O (P < 0.05). The f dependences of EL and Rti were increased by edema (P < 0.05), and there was a large negative dependence of EL on VT at Paw = 14 cmH2O. Edema increased RL (P < 0.05), but this increase depended on f, VT, and Paw. The increase in RL was due largely to increases in Rti at Paw = 14 cmH2O and to increases in Raw at Paw = 11 cmH2O. We conclude that the functional effects of oleic acid-induced pulmonary edema on RL are due mostly to changes in lung tissue.
肺水肿如何影响肺组织和气道特性尚不清楚。通过测量气道压力和流量，我们在5只麻醉麻痹、开胸的犬正常呼吸频率（f）和潮气量（VT）范围内进行正弦波刺激时，测量了肺弹性（EL）和阻力（RL）。通过粘贴在肺表面的胶囊测量肺泡压力，将RL分为组织成分（Rti）和气道成分（Raw）。在右心房注射油酸诱导严重肺水肿后，在与对照动物相同的平均气道压力（Paw）（11 cmH2O）以及更高的Paw（14 cmH2O）下重复刺激，这是闭胸犬在水肿期间会出现的情况（G.M.巴纳斯、D.斯塔梅诺维奇和K.R.卢琴。《应用生理学杂志》73:1040 - 1046，1992）。水肿增加了EL，且在Paw = 14 cmH2O时这种增加更大（P < 0.05）。水肿增加了EL和Rti对f的依赖性（P < 0.05），并且在Paw = 14 cmH2O时EL对VT有很大的负依赖性。水肿增加了RL（P < 0.05），但这种增加取决于f、VT和Paw。RL的增加在很大程度上是由于在Paw = 14 cmH2O时Rti增加，以及在Paw = 11 cmH2O时Raw增加。我们得出结论，油酸诱导的肺水肿对RL的功能影响主要归因于肺组织的变化。
