Tissue inflammation without bacteria produces increased oxygen consumption and distant organ lipid peroxidation.
An inflammatory focus was produced by implantation of gauze below the hide in the flanks of six sheep with flank lymph fistulas. Physiologic and metabolic parameters were monitored in the unanesthetized animals for 7 days, after which the gauze was removed and monitoring continued for another 5 days. Animals were then killed. Lung and liver tissue was inspected and analyzed for lipid peroxide content. Data were compared with those of six controls in which gauze was not implanted. We noted a transient significant increase (on day 1 only) in wound lymph, thromboxane B2, and 6-keto-PGF1 alpha from baseline values of 190 +/- 70 and 20 +/- 10 pg/ml to 1000 +/- 240 and 420 +/- 70 pg/ml, respectively. Plasma values were also significantly increased on day 1. Body temperature increased by 1 degree C and cardiac index increased by 30% during this period, whereas oxygen consumption, VO2, was not significantly increased. The VO2 and cardiac index increased by 50% over baseline, beginning on day 5, whereas systemic vascular resistance decreased. Body temperature was not increased. These changes corresponded with an increase in wound lymph monocyte count from 0% to 15% of total. The VO2 and cardiac index remained increased after gauze removal. No bacteria were found in the wound. Postmortem analysis revealed a marked monocyte-macrophage infiltration in both lung and liver. Lung water, represented as water content over dry weight, was normal. Lung and liver lipid peroxidation, measured by the by-product malondialdehyde content, increased 300% and 90% over control values, respectively. We conclude that a local, nonbacteria-induced wound inflammation increases VO2, with the increase not corresponding to increase in body temperature. Distant organ changes, namely, changes in lung and liver, were also evident 5 days after gauze removal.
Lalonde
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C
Longwood Area Trauma Center, Harvard Medical School, Boston, MA 02115.
Demling
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RH
Goad
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ME
D000818:Animals; D002056:Burns / Q000503:physiopathology; D004195:Disease Models, Animal; D005260:Female; D006439:Hemodynamics; D007249:Inflammation / Q000473:pathology / Q000503:physiopathology*; D008054:Lipid Peroxides / Q000378:metabolism*; D008168:Lung / Q000473:pathology; D010101:Oxygen Consumption; D011453:Prostaglandins / Q000097:blood; D012756:Sheep
D008054:Lipid Peroxides; D011453:Prostaglandins