Blomqvist H, Berg B, Frostell C, Wickerts C J, Hedenstierna G
Department of Anaesthesia and Intensive Care, Danderyd Hospital, Sweden.
Acta Anaesthesiol Scand. 1990 Jul;34(5):377-83. doi: 10.1111/j.1399-6576.1990.tb03106.x.
Net fluid leakage (LN) from the intravascular to the extravascular pulmonary space was estimated in anaesthetised dogs after injection of oleic acid (OA) (n = 8), or after hydrostatic pressure elevation by inflation of a left atrial balloon (n = 5). LN was calculated as the sum of: (i) rate of change in extravascular lung water (delta EVLW), (ii) thoracic lymph flow, and (iii) pleural fluid formation per time unit. Pleural fluid formation was measured in five dogs with hydrostatic or OA induced pulmonary oedema and was 1.8 +/- 0.9 ml/kg/h. In OA-induced pulmonary oedema, LN increased to a peak of 9.2 ml/kg/h within 2 h after OA injection. Thereafter LN fell and was 2-4 ml/kg/h during the succeeding 2-4 h. During hydrostatic pulmonary oedema LN was increased to as much as 13 ml/kg/h, but it became negative, -5 to -8 ml/kg/h (reabsorption of extravascular fluid) as soon as pulmonary vascular pressures returned to normal following deflation of the left atrial balloon. We conclude that in both forms of oedema there is an initial rapid leakage. In OA-induced oedema this leakage continues, although at a slower rate, whereas in hydrostatic oedema there is a considerable net fluid absorption from the pulmonary extravascular to the intravascular space as soon as vascular pressures are brought to normal levels.
在麻醉犬中，通过注射油酸（OA）（n = 8）或通过左心房球囊充气升高静水压（n = 5）来估计从血管内到血管外肺间隙的净液体渗漏（LN）。LN的计算方法为：（i）血管外肺水变化率（δEVLW）、（ii）胸淋巴流量和（iii）每单位时间的胸腔积液形成量之和。在五只因静水压或OA诱导肺水肿的犬中测量了胸腔积液形成量，为1.8±0.9 ml/kg/h。在OA诱导的肺水肿中，LN在注射OA后2小时内增加到峰值9.2 ml/kg/h。此后LN下降，在随后的2 - 4小时内为2 - 4 ml/kg/h。在静水压性肺水肿期间，LN增加到高达13 ml/kg/h，但一旦左心房球囊放气后肺血管压力恢复正常，LN就变为负值，即 -5至 -8 ml/kg/h（血管外液体重吸收）。我们得出结论，在两种形式的水肿中都存在初始快速渗漏。在OA诱导的水肿中，这种渗漏会持续，尽管速度较慢，而在静水压性水肿中，一旦血管压力恢复到正常水平，就会有大量的液体从肺血管外间隙净吸收到血管内间隙。
