Induction of procalcitonin and proinflammatory cytokines in an anhepatic baboon endotoxin shock model
Induction of procalcitonin and proinflammatory cytokines in an anhepatic baboon endotoxin shock model
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DOI：
10.1097/00024382-200302000-00017
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发表时间：
2003-02-01
期刊：
影响因子：
3.1
通讯作者：
Redl, H
中科院分区：
文献类型：
--
作者：
Meisner, M;Müller, V;Redl, H
我们的目的是评估肝脏在狒狒内毒素休克模型中降钙素原（PCT）和细胞因子诱导中的作用。在静脉注射内毒素（100杯/千克LPS大肠杆菌）诱发内毒素休克之前，在狒狒中建立了完全肝切除和门静脉吻合。两只未经手术干预的狒狒作为对照。测定术前、术后及内毒素给药后6小时血浆PCT、肿瘤坏死因子(TNF)- α、白细胞介素（IL） 6、IL-8、内毒素、血流动力学和代谢参数的浓度。6小时后，PCT浓度在对照动物中分别升高至1.2和4.6 ng/mL，但在无肝狒狒中仍低于0.3 ng/mL。在对照组中，IL-6和IL-8仅在数小时内升高，但在去肝动物中，IL-6和IL-8仍保持升高，接近最大值（il - 6,2 -6 ng/mL）或数倍高（il - 8,30 -35 ng/mL），而tnf - α反应仅为对照组的一小部分（0.3 ng/mL）。与对照组相比，去肝动物的内毒素含量更高，持续时间更长。无肝狒狒几乎不产生PCT，这表明在内毒素休克期间，肝脏是PCT产生的主要来源。此外，肝脏似乎也是tnf - α的重要来源，而不是IL-6或IL-8。
Our objective was to evaluate the role of the liver for procalcitonin (PCT) and cytokine induction in a baboon endotoxin shock model. Complete liver resection with portocaval anastomosis was established in a baboon prior to the induction of endotoxin shock by intravenous administration of endotoxin (100 mug/kg LPS Escherichia coli). Two baboons without surgical intervention were used as controls. Plasma concentrations of PCT, tumor necrosis factor (TNF)-alpha, interleukin (IL) 6, IL-8, endotoxin, and hemodynamic and metabolic parameters were measured pre- and postoperatively and until 6 h after endotoxin administration. PCT concentrations increased to 1.2 and 4.6 ng/mL in control animals at 6 h, but remained below 0.3 ng/mL in the anhepatic baboon. IL-6 and IL-8 increased only for few hours in controls, but remained elevated in the hepatectomized animal near their maximum (IL-6, 2-6 ng/mL) or several-fold higher (IL-8, 30-35 ng/mL), whereas TNF-alpha response was only a small fraction (0.3 ng/mL) of the controls. Endotoxin was much higher and longer persisting in the hepatectomized animal compared with controls. The near absence of PCT production in the anhepatic baboon suggests a primary role for the liver as a source of PCT production during endotoxin shock. Furthermore, the liver also seems to be an important source of TNF-alpha, but not IL-6 or IL-8.