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Abstract
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.
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ratio.Article info
Publication history
Accepted:
March 4,
1982
Footnotes
☆Supported by NIH grants HL 25403, HL 07013, and GM 27619.
Identification
Copyright
© 1982 Published by Elsevier Inc.
