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Catherine Wong, MD; John Flynn, PhD; Robert H. Demling, MD

Arch Surg. 1984;119(1):77-82.

Abstract
• We tested the hypothesis that the increased permeability in the pulmonary microcirculation seen with endotoxin is caused by the release of oxygen radicals from activated neutrophils. We first compared the pulmonary injury in sheep caused by low-dose endotoxin with that produced by phorbol myristate acetate, an agent that selectively causes the release of oxygen radicals from neutrophils. We then determined the degree of lung tissue lipid peroxidation, a reflection of direct oxygen radical damage after endotoxin and phorbol myristate acetate. Both agents produced a nearly identical increase in protein permeability; however, peroxidation was only evident with phorbol myristate acetate. Higher doses of endotoxin did result in increased lung peroxidation as well as a more severe physiologic injury. We can conclude that oxygen radical release, most likely from neutrophils, occurs with endotoxin. However, the permeability injury may not be the direct result of increased lipid peroxidation, as increased permeability can be seen without measurable increases in this parameter.

(Arch Surg 1984;119:77-82)

Author Affiliations
From the Department of Surgery, University of California-Davis (Dr Wong); Jefferson Medical College, Philadelphia (Dr Flynn); and the Longwood Area Trauma Center, Harvard Medical School, Boston (Dr Demling).

Footnotes
Accepted for publication Sept 7, 1983.

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

Reprint requests to Longwood Area Trauma Center, 75 Francis St, Boston, MA 02115 (Dr Demling).

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