Abstract
Noncardiogenic edema fluid often contains high levels of plasma proteins, which may inhibit the function of the lung surfactant complex and thus decrease interstitial hydrostatic pressures. We questioned whether, in the awake and standing animal, displacement of the alveolar surface lining would alter the permeability of the thin and sparsely supported pulmonary capillaries. Sheep prepared with lung lymph-fistulae were given an aerosolized detergent (Det) to displace the lung surfactant complex. After the sheep were given Det, protein flux was significantly increased (P < 0.05). To validate the suggested permeability increase, pulmonary vein occluders were surgically implanted and experiments repeated with pulmonary arterial pressures elevated 10 mmHg above baseline. After 2 h of elevated pulmonary arterial pressure, lung lymph increased fivefold. At this time, lymph-to-plasma total protein concentration ratios for air and saline-plus- ethanol vehicle were significantly lower (P < 0.01) than baseline ratios (0.26 ± 0.06 and 0.34 ± 0.07, respectively). No significant difference could be shown in lymph-to-plasma ratios after the sheep were given Det. We conclude that disruption of the alveolar lining can cause a detectable increase in protein flux due, in part, to an increase in microvascular permeability.
Original language | English (US) |
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Pages (from-to) | 1016-1023 |
Number of pages | 8 |
Journal | Journal of Applied Physiology |
Volume | 74 |
Issue number | 3 |
DOIs | |
State | Published - 1993 |
Externally published | Yes |
Keywords
- alveolar surface tension
- lung lymph flow
- lung water
- lymph-to-plasma barrier
- protein flux
- pulmonary edema
ASJC Scopus subject areas
- General Medicine