Thermal Injury Alters Endothelial Vasoconstrictor and Vasodilator Response to Endotoxin

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Abstract
The unique location of the endothelium makes it vulnerable to injury from circulating factors created at remote wounds. In this study, we examined the effect of a sequential burn and lipopolysaccharide (LPS) challenge on endothelial function in vitro. Human umbilical vein endothelial cells treated with 20% human serum isolated from burn patients (>40% total burn surface area) at 2 and 24 hours postinjury. Cultures were subsequently treated with Escherichia coli LPS:0111:B4 (0.10-100ng/mL). Endothelin-1 (ET-1), 6-ketoPGF1a, and NO2/NO3 were detected by using specific enzyme immunoassays. Burn serum did not alter endothelial ET-1, PGI2, or NO secretion compared with Control serum. LPS significantly enhanced 6-ketoPGF1a (54,242 ± 14,466 pg/106 cells) and NO2/NO3 (723 ± 210 μM) secretion, but not ET-1 compared with Control serum alone (3,878 ± 963 and 219 ± 110). Burn serum pretreatment significantly enhanced the ET-1 response to LPS (303 ± 36 pg/106 cells vs. 193 ± 47). The 6-ketoPGF1a (16,509 ± 3,785) and NO2/NO3 (354 ± 98) responses to Burn/LPS were significantly diminished compared with Control/LPS. Although this level of 6-ketoPGF1a was elevated compared with Control alone (7,518 ± 2,299), NO2/NO3 was unchanged (significance at p Thermal injury may prime remote endothelium and alter the response to a septic focus with an enhanced vasoconstrictor (ET-1) and diminished vasodilator (PGI2/NO) response, a situation that may contribute to postburn distal organ injury.

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