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John Mihran Davis, MD; Roger W. Yurt, MD; Philip S. Barie, MD; Lisa C. Hudgins, MD; Madhu Verma, MA; Peter Dineen, MD; G. Tom Shires, MD

Arch Surg. 1989;124(12):1451-1455.

Abstract
• We investigated the cause of the reduced leukotriene B₄ (LTB₄) production seen in neutrophils from patients with established adult respiratory distress syndrome compared with control neutrophils. Lymphocytes/monocytes from controls were found to synergistically enhance the amount of LTB₄ produced when incubated with neutrophils. This synergistic effect was not seen in cells from patients with adult respiratory distress syndrome. Fatty-acid analysis of neutrophils from patients with adult respiratory distress syndrome and controls showed remarkable similarity in all quantities of fatty acids measured except for arachidonic acid, where there was a 22% reduction in patients' cells compared with controls. Assay of the rate of generation of LTB₄ and its degradation product, 20-hydroxy LTB₄, revealed that reduced LTB₄ generation in patients' neutrophils was not due to increased degradation of LTB₄ by hydroxylase enzymes. When the amount of LTB₄ being generated per milliliter of whole blood was analyzed in the patients with adult respiratory distress syndrome and compared with controls, it was determined that the potential to generate LTB₄ in patients in the intensive care unit was three to five times greater than in controls.

(Arch Surg. 1989;124:1451-1455)

Author Affiliations
From the Department of Surgery, Cornell University Medical College (Drs Davis, Yurt, Barie, Hudgins, Dineen, and Shires, and Ms Verma), and Rockefeller University (Dr Hudgins), New York, NY.

Footnotes
Accepted for publication August 2, 1989.

Read before the Ninth Annual Meeting of the Surgical Infection Society, Denver, Colo, April 14, 1989.

Reprint requests to Department of Surgery, Cornell University Medical College, 1300 York Ave, New York, NY 10021 (Dr Davis).

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