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Richard H. Carmona, MD; Tanny C. Tsao, MS; Donald D. Trunkey, MD

Arch Surg. 1984;119(2):189-192.

Abstract
• Prostacyclin, or prostaglandin I₂ (PGI₂), and thromboxane A₂ (TXA₂) are potent, endogenously produced, vasoactive substances that have been implicated as mediators in the pathophysiologic nature of septic shock. We investigated the contribution and production of PGI₂ and TXA₂ in sepsis and septic shock, using an intact rabbit model and an in vitro rabbit isolated cardiac perfusion model. Continuous hemodynamic monitoring of both experimental models, along with serial radioimmunoassays of the metabolites of PGI₂ and TXA₂, indicated that myocardial depression is a common finding in subjects with septic shock and that septic shock causes a suppression of PGI₂ production while augmenting TXA₂ production. In addition, PGI₂ and TXA₂ were mediators of some cardiovascular changes in septic shock but were themselves not the toxic factor(s) responsible for the associated myocardial depression.

(Arch Surg 1984;119:189-192)

Author Affiliations
From the University of California—San Francisco Medical School and the Department of Surgery, San Francisco General Hospital.

Footnotes
Accepted for publication Sept 16, 1983.

Read before the Third Annual Meeting of the Surgical Infection Society, Fort Lauderdale, Fla, May 10, 1983.

Reprint requests to Surgical Service, San Francisco General Hospital, San Francisco, CA 94110 (Dr Trunkey).

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