Objective To study the change in serum levels of soluble CD14, tumor necrosis factor-α, E-selectin, interleukin-10 and mean arterial pressure, as well as their relationship to infection during the pathophysiologic process in endotoxemia of rabbits.
Methods Sixteen rabbits were randomly divided into two groups: group A, as a control group; group B, endotoxemia group. The model of rabbit with endotoxemia were used. Endotoxin at a dose of 1.5 mg/(kg·h) or 3 mg/(kg·h) was continuously infused through external jugular vein within 2 hours, 1 hour respectively. The change of levels of serum soluble CD14, tumor necrosis factor-α, interleukin-10 and E-selectin were observed at 0 (time before infusion of endotoxin), 30, 60, 120, 180, 240, 300 minutes, while mean arterial pressure was measured by polygraphy system.
Results In the group B,there was an increase of content of soluble CD14,tumor necrosis factor-α,interleukin-10 and E-selectin following 30, 120 minutes respectively,and mean arterial pressure was lower than that of group A at same time points.
Conclusion The results suggest that soluble CD14,tumor necrosis factor-α,interleukin-10 and E-selectin may play an important role during the change of infection and that these changes may be closely related with severe infection.
Citation:
YANG Yong,SHI De. Dynamics of Serum Levels of Soluble CD14,E-selectin and Interleukin-10 in Rabbits with Endotoxemia. CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY, 2002, 9(1): 10-12. doi:
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黄青青,杨镛,万林骏,等.复方丹渗注射液对兔内毒素休克的防治作用 [J]. 中国危重病急救医学,1998; 10(4)∶ 227.
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Haziot A, Rong GW, Bazil V, et al. Recombinant soluble CD14 inhibits LPSinduced tumor necrosis factorα production by cells in whole blood [J]. J Immunol, 1994; 152(11)∶5868.
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Haziot A, Rong GW, Lin XY, et al. Recombinant soluble CD14 prevents mortality in mice treated with endotoxin (Lipopolysaccharide) [J]. J Immunol, 1994; 152(12)∶6529.
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Bevilacqua MP, Stengelin S, Gimbrane MA, et al. Endothelial leukocyte adhesion molecule1: an inducible receptor for new trophils related to complement regulatory protein and lectin [J]. Science, 1989; 243(12)∶ 1160.
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Bogdan C, Vodovota Y, Nathan C. Macrophage deactivation by interleukin10 [J]. J Exp Med, 1991; 174(9)∶1549.
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Hickey MJ, Issekutz AC, Reinhardt PH, et al. Endogenous interleukin10 regulates hemodynamic parameters, leukocyteendothelial cell interactions, and microvascular permeability during endotoxemia [J]. Cir Res, 1998; 83(10)∶1124.
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Gerard C, Bruyns C, Marchant A, et al. Interleukin10 reduces the release of tumor necrosis factor and prevents lethality in experimental endotoxemia [J]. J Exp Med, 1993; 177(3)∶547.
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Mayadas TN, Johnson RC, Rayburn H, et al. Leukocyte rolling and extravasation are severely comproised in Pselectindeficient mice [J]. Cell, 1993; 74(4)∶541.
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- 1. 黄青青,杨镛,万林骏,等.复方丹渗注射液对兔内毒素休克的防治作用 [J]. 中国危重病急救医学,1998; 10(4)∶ 227.
- 2. Haziot A, Rong GW, Bazil V, et al. Recombinant soluble CD14 inhibits LPSinduced tumor necrosis factorα production by cells in whole blood [J]. J Immunol, 1994; 152(11)∶5868.
- 3. Haziot A, Rong GW, Lin XY, et al. Recombinant soluble CD14 prevents mortality in mice treated with endotoxin (Lipopolysaccharide) [J]. J Immunol, 1994; 152(12)∶6529.
- 4. Bevilacqua MP, Stengelin S, Gimbrane MA, et al. Endothelial leukocyte adhesion molecule1: an inducible receptor for new trophils related to complement regulatory protein and lectin [J]. Science, 1989; 243(12)∶ 1160.
- 5. Bogdan C, Vodovota Y, Nathan C. Macrophage deactivation by interleukin10 [J]. J Exp Med, 1991; 174(9)∶1549.
- 6. Hickey MJ, Issekutz AC, Reinhardt PH, et al. Endogenous interleukin10 regulates hemodynamic parameters, leukocyteendothelial cell interactions, and microvascular permeability during endotoxemia [J]. Cir Res, 1998; 83(10)∶1124.
- 7. Gerard C, Bruyns C, Marchant A, et al. Interleukin10 reduces the release of tumor necrosis factor and prevents lethality in experimental endotoxemia [J]. J Exp Med, 1993; 177(3)∶547.
- 8. Mayadas TN, Johnson RC, Rayburn H, et al. Leukocyte rolling and extravasation are severely comproised in Pselectindeficient mice [J]. Cell, 1993; 74(4)∶541.