Abstract

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.

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