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J Appl Physiol 96: 25-31, 2004. First published May 2, 2003; doi:10.1152/japplphysiol.01074.2002
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Recombinant plasma gelsolin infusion attenuates burn-induced pulmonary microvascular dysfunction

Patricia A. Rothenbach,1,* Benny Dahl2,1,* Jason J. Schwartz,1,* Grant E. O'Keefe,1 Masaya Yamamoto,3 William M. Lee4, Jureta W. Horton,1 Helen L. Yin,3 and Richard H. Turnage1

Departments of 1Surgery, 3Physiology, and 4Internal Medicine, University of Texas Southwestern Medical School and the Veterans Affairs North Texas Health Care System, Dallas, Texas 75216; and 4Department of Orthopaedic Surgery, Rigshospitalet, University Hospital of Copenhagen, Copenhagen, Denmark

Submitted 15 November 2002 ; accepted in final form 17 April 2003

Reduced plasma concentrations of the extracellular actin-binding proteins gelsolin and Gc-globulin correlate with pulmonary failure and death in humans after injury. The purpose of this study was to investigate the role of plasma gelsolin in the pathophysiology of inflammation-induced lung injury. We postulated that plasma gelsolin levels decrease at an early time point after burn injury and that the intravenous infusion of gelsolin prevents burn-induced pulmonary microvascular dysfunction. Adult Sprague-Dawley rats were randomized to undergo a 40% body surface area thermal injury (Burn) or manipulation without burn (Sham). Plasma gelsolin and Gc-globulin concentrations were determined at various times during the first 6 days of injury by Western blotting. Other animals were randomized to receive either recombinant human gelsolin (0.078, 0.78, or 7.8 mg) or albumin (7.8 mg) before and 8 h after Burn or Sham. Twenty-four hours later, pulmonary microvascular permeability was assessed by measuring the capillary filtration by use of an isolated, perfused lung model. We found that plasma gelsolin levels of burn-injured rats decreased to 10% of normal levels within 12 h and remained below normal levels for up to 6 days postinjury. Gc-globulin values also fall, but to a lesser extent and only transiently. Treatment of burned animals with intravenous infusions of recombinant human gelsolin prevented the increase in pulmonary microvascular permeability that accompanies this injury. Our findings are consistent with the hypothesis that plasma gelsolin depletion contributes to the pathophysiology of pulmonary microvascular dysfunction during inflammation.

Gc-globulin; microvascular permeability; capillary filtration coefficient; isolated perfused lung model


Address for reprint requests and other correspondence: R. H. Turnage, Professor and Chairman, Dept. of Surgery, LSU Health Sciences Center School of Medicine, 1501 Kings Highway, PO Box 33932, Shreveport, LA 71130-3932 (E-mail rturna{at}lsuhsc.edu).




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