Re-expansion pulmonary edema. A potential role for free radicals in its pathogenesis

Robert Jackson, C. F. Veal, C. B. Alexander, A. L. Brannen, J. D. Fulmer

Research output: Contribution to journalArticle

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Abstract

Re-expansion pulmonary edema (RPE) has been atributed to decreased lung interstitial pressures from a variety of mechanisms. Because some recent studies have implicated mechanisms that increase microvascular permeability in RPE, we tested whether the edema were due to free radical generation during re-expansion and reoxygenation of the collapsed lung. We used a rabbit model of RPE to test the effects of intracellular (dimethylthiourea) or extracellular (catalase) oxygen metabolite scavengers. Allopurinol was administered separately to determine whether xanthine oxidase was an important source of superoxide in this model. Edema was quantitated both gravimetrically and histologically, and lung xanthine oxidase activity was measured using a sensitive fluorometric assay with pterin as substrate. The results suggest indirectly that OH· or H2O2 (derived from O2-) contribute to the well-documented increase in lung permeability in RPE because dimethylthiourea, dimethylthiourea plus catalase, or catalase alone inhibited the edema to various degrees. Further, we observed histologically that increased numbers of neutrophils were present in re-expanded lungs and that neutrophil infiltration appeared to be diminished by antioxidation administration. Allopurinol did not decrease the edema, because xanthine oxidase activity in rabbit lung tissue is extremely low. We speculate that free radical generation in lung tissue contributes to the pathogenesis of RPE, although reinitiation of lung perfusion and ventilation requires a rapid change in intrathoracic pressure.

Original languageEnglish
Pages (from-to)1165-1171
Number of pages7
JournalAmerican Review of Respiratory Disease
Volume137
Issue number5
StatePublished - Jan 1 1988
Externally publishedYes

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Pulmonary Edema
Free Radicals
Lung
Xanthine Oxidase
Edema
Catalase
Allopurinol
Pterins
Rabbits
Pressure
Neutrophil Infiltration
Capillary Permeability
Superoxides
Ventilation
Permeability
Neutrophils
Perfusion
Oxygen
1,3-dimethylthiourea

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

Cite this

Jackson, R., Veal, C. F., Alexander, C. B., Brannen, A. L., & Fulmer, J. D. (1988). Re-expansion pulmonary edema. A potential role for free radicals in its pathogenesis. American Review of Respiratory Disease, 137(5), 1165-1171.

Re-expansion pulmonary edema. A potential role for free radicals in its pathogenesis. / Jackson, Robert; Veal, C. F.; Alexander, C. B.; Brannen, A. L.; Fulmer, J. D.

In: American Review of Respiratory Disease, Vol. 137, No. 5, 01.01.1988, p. 1165-1171.

Research output: Contribution to journalArticle

Jackson, R, Veal, CF, Alexander, CB, Brannen, AL & Fulmer, JD 1988, 'Re-expansion pulmonary edema. A potential role for free radicals in its pathogenesis', American Review of Respiratory Disease, vol. 137, no. 5, pp. 1165-1171.
Jackson, Robert ; Veal, C. F. ; Alexander, C. B. ; Brannen, A. L. ; Fulmer, J. D. / Re-expansion pulmonary edema. A potential role for free radicals in its pathogenesis. In: American Review of Respiratory Disease. 1988 ; Vol. 137, No. 5. pp. 1165-1171.
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