Acute versus sustained hypoproteinemia and posttraumatic pulmonary edema.

We compared the effect of an acute protein depletion versus a sustained protein depletion on pulmonary edema formation. Acute hypoproteinemia was produced either by a rapid plasmapheresis or as the result of acute hemorrhagic shock and resuscitation. Sustained hypoproteinemia was produced by a 24-hour plasmapheresis or as the 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 twofold to threefold 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 seen in a nonshocked animal with a comparable protein depletion. With restoration of the plasma-lymph oncotic gradient, the lymph flow returned to baseline. The lymph protein content always exceeded 2 gm/dl. In the sustained depletion groups the lymph flow also increased twofold to threefold but remained elevated for over 48 hours 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 below 2 gm/dl, indicating a significant interstitial protein depletion. We conclude that 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.