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Comparing hemodynamics, blood gas analyses and proinflammatory cytokines in endotoxemic and severely septic rats.

机译:比较内毒素血症和严重脓毒症大鼠的血流动力学,血气分析和促炎细胞因子。

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Lipopolysaccharide (LPS) is often used in short-term models of inflammation. Since endotoxemia and sepsis are different entities we have recently established a short-term sepsis model in rats induced by cecal ligation and incision (CLI). This retrospective study was conducted in order to identify similarities and differences between both experimental approaches. 32 anesthetized/ventilated male rats from the following four groups were analysed (each n=8): CTRL-group (0.9% NaCl i.v.); LPS-group (5mg/kg i.v.); SHAM-group (laparotomy); CLI-group (1.5 cm blade incision). Mean arterial blood pressure (MAP) and blood gas parameters (arterial base excess (BE) and pH) were continuously recorded. Total observation time was 300 min. Plasma samples were obtained afterwards. LPS and CLI induced significant arterial hypotension and metabolic acidosis compared to CTRL- or SHAM-group, respectively. Yet, between the LPS- and CLI-groups, there were no differences in MAP, BE and pH. LPS significantly induced IL-1beta, IL-6 and TNF-alpha in the plasma. In contrast, CLI showed a clear tendency towards increased IL-1beta and IL-6 plasma levels and did not affect TNF-alpha. Our results indicate that the CLI sepsis model is suitable for short-term investigations on hemodynamic alterations and blood gas analyses during sepsis. 300 min after the proinflammatory insult, plasma concentrations of IL-1beta and IL-6 in the plasma remain considerably lower after CLI compared to endotoxemia. Low TNF-alpha concentrations 300 min after sepsis induction could be interpreted as considerable immunosuppression during CLI sepsis.
机译:脂多糖(LPS)通常用于炎症的短期模型。由于内毒素血症和败血症是不同的实体,我们最近在盲肠结扎切开术(CLI)诱导的大鼠中建立了短期脓毒症模型。进行这项回顾性研究是为了确定两种实验方法之间的异同。分析来自以下四组的32只麻醉/通风的雄性大鼠(每组n = 8):CTRL-组(0.9%NaCl静脉); LPS组(静脉内5mg / kg);假手术组(开腹手术); CLI组(1.5厘米刀片切口)。连续记录平均动脉血压(MAP)和血气参数(动脉基础过量(BE)和pH)。总观察时间为300分钟。之后获得血浆样品。与CTRL组或SHAM组相比,LPS和CLI分别引起明显的动脉低血压和代谢性酸中毒。但是,在LPS组和CLI组之间,MAP,BE和pH值没有差异。 LPS显着诱导血浆中的IL-1beta,IL-6和TNF-α。相反,CLI显示出明显的增加IL-1beta和IL-6血浆水平的趋势,并且不影响TNF-α。我们的结果表明,CLI脓毒症模型适合于脓毒症期间血流动力学改变和血气分析的短期研究。促炎性损伤后300分钟,与内毒素血症相比,CLI后血浆中IL-1beta和IL-6的血浆浓度仍显着降低。脓毒症诱导后300分钟的低TNF-α浓度可解释为CLI脓毒症期间相当大的免疫抑制。

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