ACUTE VERSUS SUSTAINED HYPOPROTEINEMIA AND POST-TRAUMATIC PULMONARY-EDEMA

  • 1 January 1982
    • journal article
    • research article
    • Vol. 92  (1) , 79-86
Abstract
The effect was studied of an acute protein depletion vs. a sustained protein depletion on pulmonary edema formation. Acute hypoproteinemia was produced by a rapid plasmapheresis or as the result of acute hemorrhagic shock and resuscitation. Sustained hypoproteinemia was produced by a 24-h plasmapheresis or as a result of a 50% body burn. Unanesthetized sheep with lung lymph fistulas were used as the experimental model. In the acute depletion groups an early 2- to 3-fold increase in lymph flow was seen, reflecting an increase in fluid flux, across the microcirculation, with the increase in lymph flow after resuscitation from shock being identical to that in a nonshocked animal with a comparable protein depletion. With restoration of the plasma-lymph oncotic gradient, the lymph flow returned to baseline. Lymph protein content always exceeded 2 g/dl. In the sustained depletion groups the lymph flow also increased 2- to 3-fold but remained elevated for > 48 h despite a rapid restoration of plasma-lymph oncotic gradient. The increase in fluid flux after burn was identical to that after protein depletion alone. In these groups the lymph protein content was < 2 g/dl, indicating a significant interstitial protein depletion. A marked increase in fluid flux is seen after sustained protein depletion that is unrelated to oncotic pressure. This process appears to be related to the degree of washout of interstitial protein, possibly decreasing the viscosity of the interstitial matrix, leading to a more rapid edema formation.