Pinto Carolina Ferreira, Watanabe Mirian, da Fonseca Cassiane Dezoti, Ogata Cecília Ide, Vattimo Maria de Fátima Fernandes
Doutoranda da Escola de Enfermagem, Universidade de São Paulo, São Paulo, SP, Brasil.
Rev Esc Enferm USP. 2012 Oct;46 Spec No:86-90. doi: 10.1590/s0080-62342012000700013.
Sepsis associated with multiple organ failure such as acute kidney injury (AKI) shows a high mortality rate in critically ill patients. This study investigated the sepsis induced AKI in experimental models. Adult, males, Wistar rats divided into the following groups: Control-surgical control and Sepsis-sepsis induction for the cecal ligation and puncture (CLP). Physiological parameters (rectal temperature, mean arterial pressure-MAP, serum glucose and urinary flow); renal function (creatinine clearance); oxidative stress (urinary peroxides and thiobarbituric acid reactive substances-TBARS) and kidney histological analysis were evaluated. That study concludes that sepsis induces AKI by endothelial injury with hemodynamic dysfunction, release of inflammatory mediators and reactive oxygen species (ROS) generation by tubular cells, in an association of renal vasoconstriction due to hemodynamic and inflammatory disturbances.
与多器官衰竭相关的脓毒症，如急性肾损伤（AKI），在危重症患者中显示出高死亡率。本研究在实验模型中研究了脓毒症诱导的急性肾损伤。成年雄性Wistar大鼠分为以下几组：对照组——手术对照组和脓毒症组——通过盲肠结扎和穿刺（CLP）诱导脓毒症。评估了生理参数（直肠温度、平均动脉压-MAP、血清葡萄糖和尿流）；肾功能（肌酐清除率）；氧化应激（尿过氧化物和硫代巴比妥酸反应性物质-TBARS）以及肾脏组织学分析。该研究得出结论，脓毒症通过内皮损伤导致急性肾损伤，伴有血流动力学功能障碍、炎症介质释放以及肾小管细胞产生活性氧（ROS），这是由血流动力学和炎症紊乱导致的肾血管收缩共同作用的结果。
