TY - JOUR
T1 - Thermal injury alters endothelial vasoconstrictor and vasodilator response to endotoxin
AU - Murphy, Joseph T.
AU - Duffy, Steven
AU - Purdue, Gary F.
AU - Hunt, John L.
PY - 1999/9/1
Y1 - 1999/9/1
N2 - Background: 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. Methods: 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-ketoPGF(1a), and NO2/NO3 were detected by using specific enzyme immunoassays. Results: Burn serum did not alter endothelial ET-1, PGI2, or NO secretion compared with Control serum. LPS significantly enhanced 6-ketoPGF(1a) (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-ketoPGF(1a) (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- ketoPGF(1a) was elevated compared with Control alone (7,518 ± 2,299), NO2/NO3 was unchanged (significance at p < 0.05). Conclusion: 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.
AB - Background: 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. Methods: 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-ketoPGF(1a), and NO2/NO3 were detected by using specific enzyme immunoassays. Results: Burn serum did not alter endothelial ET-1, PGI2, or NO secretion compared with Control serum. LPS significantly enhanced 6-ketoPGF(1a) (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-ketoPGF(1a) (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- ketoPGF(1a) was elevated compared with Control alone (7,518 ± 2,299), NO2/NO3 was unchanged (significance at p < 0.05). Conclusion: 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.
KW - Endothelial cell
KW - Endotoxin
KW - Permeability
KW - Thermal injury
KW - Vasoactivity
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U2 - 10.1097/00005373-199909000-00010
DO - 10.1097/00005373-199909000-00010
M3 - Article
C2 - 10498303
AN - SCOPUS:0032862314
SN - 1079-6061
VL - 47
SP - 492
EP - 499
JO - Journal of Trauma - Injury, Infection and Critical Care
JF - Journal of Trauma - Injury, Infection and Critical Care
IS - 3
ER -