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J Thorac Cardiovasc Surg 1998;115:631-637
© 1998 Mosby, Inc.

CARDIAC AND PULMONARY REPLACEMENT

Addition Of A Mast Cell Stabilizing Compound To Organ Preservation Solutions Decreases Lung Reperfusion Injury

This work was supported by a grant (M.L.B.) from the Heart and Lung Surgery Foundation, Los Angeles, Calif.

Read at the Twenty-third Annual Meeting of The Western Thoracic Surgical Association, Napa, Calif., June 25-28, 1997.

Received for publication July 8, 1997; revisions requested Oct. 6, 1997; revisions received Oct. 22, 1997; accepted for publication Oct. 22, 1997. Address for reprints: Mark L. Barr, MD, Division of Cardiothoracic Surgery, University of Southern California, 1510 San Pablo St., Los Angeles, CA 90033.

Abstract

Objective: Research in lung transplant preservation has generally focused on free radicals and enzyme release from neutrophils, parenchymal cells, macrophages, and endothelium. The lung has a large resident population of mast cells that, when activated, release potent inflammatory mediators. We hypothesized that adding an inhibitor of mast cell degranulation, lodoxamide tromethamine (10 µmol/L), to Euro-Collins and University of Wisconsin preservation solutions, would decrease lung preservation injury.
Methods: Rat lungs were isolated, flushed with the respective solution, and stored at 4° C for 6 or 12 hours. The lungs were reperfused with fresh blood and ventilated with 100% oxygen. Alveolar-arterial oxygen difference, oxygen tension, capillary filtration coefficient, and compliance were determined.
Results: After 6 hours of ischemic storage: lodoxamide tromethamine–enhanced Euro-Collins solution decreased alveolar-arterial oxygen difference from 539 to 457 (p  = 0.004), increased oxygen tension from 119 to 205 mm Hg (p = 0.006), and decreased capillary filtration coefficient from 3.9 to 2.0 (p < 0.001); lodoxamide tromethamine–enhanced University of Wisconsin solution decreased alveolar-arterial oxygen difference from 546 to 317 (p  < 0.001), increased oxygen tension from 166 to 335 mm Hg (p < 0.001), and decreased capillary filtration coefficient from 3.0 to 1.7 (p < 0.001). After 12 hours of ischemic storage, lodoxamide tromethamine–enhanced Euro-Collins solution decreased alveolar-arterial oxygen difference from 588 to 485 (p < 0.001), increased oxygen tension from 100 to 161 mm Hg (p = 0.012), decreased capillary filtration coefficient from 6.2 to 2.6 (p < 0.001), and increased compliance from 0.12 to 0.21 (p < 0.001); lodoxamide tromethamine–enhanced University of Wisconsin solution decreased alveolar-arterial oxygen difference from 478 to 322 (p < 0.001), increased oxygen tension from 214 to 335 mm Hg (p < 0.001), decreased capillary filtration constant from 4.2 to 2.0 (p < 0.001), and increased compliance from 0.20 to 0.25 (p < 0.001).
Conclusions: Addition of lodoxamide tromethamine to Euro-Collins or University of Wisconsin solution results in a marked decrease in lung reperfusion injury as demonstrated by increased oxygenation, decreased microvascular permeability, and increased compliance. These results are relevant as Euro-Collins and University of Wisconsin solutions are the most common clinically used lung preservation solutions. This study also highlights the deleterious role of resident mast cells in preservation injury.

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