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Gus J. Slotman, MD; Kenneth W. Burchard, MD; Scott A. Yellin, MS; John J. Williams, MD

Arch Surg. 1986;121(3):271-274.

Abstract
• This study investigated the interaction of plasma levels of circulating prostaglandins and activated complement in clinical acute respiratory failure (ARDS). Fifty patients at risk for ARDS were followed up for up to ten days. Arterial blood gases and plasma levels of complement components C3a and C5a, thromboxane B₂ (TxB), and prostaglandin 6-keto-F₁, (PGI) and granulocyte aggregation (GA) were measured daily. Seventeen patients (34%) developed ARDS, with mortality of 41% vs 23% for patients without ARDS. Compared with patients without ARDS, the ARDS group had significantly increased plasma C3a (1,130 ±750 vs 636±368 ng/mL) and granulocyte aggregation (48 ± 10 vs 17 ± 4 percentage of the maximum light transmission [% max T]). Plasma C5a, TxB, or PGI did not change significantly with or without ARDS. No measured variable was significantly associated with mortality. Regression analysis revealed significant correlations between GA, TxB, PGI, and arterial oxygenation. Plasma C3a and GA are increased in ARDS, suggesting systemic complement activation. A complex series of interactions between the prostaglandins, complement, and GA appears to be involved in ARDS.

(Arch Surg 1986;121:271-274)

Author Affiliations
From the Department of Surgery, Brown University, and the Division of Biology and Medicine, Rhode Island Hospital (Drs Slotman, Burchard, and Williams and Mr Yellin) and the Providence Veterans Administration Medical Center (Dr Slotman).

Footnotes
Accepted for publication Oct 3, 1985.

Read before the Ninth Annual Surgical Symposium of the Association of Veterans Administration Surgeons, Tampa, Fla, May 9, 1985.

Reprint requests to Rhode Island Hospital, 593 Eddy St, Providence, RI 02903 (Dr Slotman).

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