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Acute versus sustained hypoproteinemia and posttraumatic pulmonary edema
Surgery
|July 1, 1982
Summary
Sustained protein depletion, unlike acute depletion, causes prolonged pulmonary edema. This edema is linked to interstitial protein loss, not just oncotic pressure changes, impacting fluid flux in the microcirculation.
Area of Science:
- Physiology
- Pathophysiology
- Edema Formation
Background:
- Protein depletion can lead to pulmonary edema.
- The mechanisms underlying edema formation in acute versus sustained hypoproteinemia require further clarification.
Purpose of the Study:
- To compare the effects of acute and sustained protein depletion on pulmonary edema formation in sheep.
- To investigate the role of oncotic pressure and interstitial protein in edema development.
Main Methods:
- Utilized unanesthetized sheep with lung lymph fistulas as an experimental model.
- Induced acute hypoproteinemia via plasmapheresis or hemorrhagic shock and resuscitation.
- Induced sustained hypoproteinemia through prolonged plasmapheresis or a major body burn.
Main Results:
- Acute protein depletion caused a transient increase in lung lymph flow, which normalized with restoration of oncotic pressure.
- Sustained protein depletion led to prolonged increases in lymph flow for over 48 hours, irrespective of oncotic pressure.
- Major body burns induced fluid flux similar to protein depletion alone, with lymph protein content below 2 gm/dl.
Conclusions:
- Sustained protein depletion causes significant pulmonary edema unrelated to oncotic pressure.
- Edema formation in sustained depletion may be linked to interstitial protein washout and altered interstitial matrix viscosity.
- The degree of interstitial protein depletion is a critical factor in sustained edema development.