Butler B D, Drake R E, Sneider W D, Allen S J, Gabel J C
Center for Microvascular and Lymphatic Studies, Houston, Texas 77030.
Am J Physiol. 1990 Feb;258(2 Pt 2):H395-9. doi: 10.1152/ajpheart.1990.258.2.H395.
Elevation of left atrial pressure to 25-40 mmHg causes continuous pulmonary edema formation in dog lungs. However, after 5-120 min, the rate of edema formation often increases (acceleration of edema). Acceleration of edema could be associated with an increase in microvascular membrane permeability because an increase in permeability would cause fluid to filter through the microvascular membrane more rapidly. To test the hypothesis that acceleration is associated with increased permeability, we used the continuous weight-gain technique to estimate the pulmonary microvascular membrane filtration coefficient (Kf) before and after acceleration of edema in 10 dogs. Acceleration occurred 36 +/- 38 (SD) min after elevation of left atrial pressure to 35.2 +/- 5.4 mmHg. Rate of weight gain increased from 0.47 +/- 0.17 g/min before acceleration to 0.88 +/- 0.26 g/min (P less than 0.05) after acceleration of pulmonary edema. Kf was increased from initial values of 0.058 +/- 0.027 to 0.075 +/- 0.029 ml.min-1.mmHg-1 (P less than 0.05) after acceleration. In five additional dogs we cannulated lung lymphatics and determined the lymph to plasma protein concentration ratio (CL/CP) before and after acceleration. CL/CP increased from base-line values of 0.37 +/- 0.07 to 0.44 +/- 0.06 (P less than 0.05) after acceleration. Both the increase in Kf and CL/CP data support the hypothesis that acceleration of edema is due, in part, to a slight increase in microvascular membrane permeability. However, the findings could also have been caused by an increase in interstitial conductance, washout of interstitial proteins, or alveolar flooding.
将犬的左心房压力升高至25 - 40 mmHg会导致其肺部持续形成肺水肿。然而,在5 - 120分钟后,肺水肿的形成速率常常会增加(肺水肿加速)。肺水肿加速可能与微血管膜通透性增加有关,因为通透性增加会使液体更快地透过微血管膜滤出。为了验证肺水肿加速与通透性增加相关这一假说,我们采用连续体重增加技术,对10只犬在肺水肿加速前后的肺微血管膜滤过系数(Kf)进行了估算。在左心房压力升高至35.2±5.4 mmHg后36±38(标准差)分钟出现肺水肿加速。体重增加速率从肺水肿加速前的0.47±0.17 g/分钟增加至加速后的0.88±0.26 g/分钟(P<0.05)。肺水肿加速后,Kf从初始值0.058±0.027增加至0.075±0.029 ml·min⁻¹·mmHg⁻¹(P<0.05)。在另外5只犬中,我们插管至肺淋巴管,并测定了肺水肿加速前后的淋巴与血浆蛋白浓度比(CL/CP)。CL/CP从基线值0.37±0.07增加至加速后的0.44±0.06(P<0.05)。Kf和CL/CP数据的增加均支持以下假说:肺水肿加速部分归因于微血管膜通透性的轻微增加。然而,这些发现也可能是由于间质传导性增加、间质蛋白洗脱或肺泡灌洗所致。