searching for mechanisms that matter in early septic acute kidney injury an experimental study搜索机制,在早期感染性急性肾损伤的实验研究.pdfVIP

Benes et al. Critical Care 2011, 15:R256 /content/15/5/R256 RESEARCH Open Access Searching for mechanisms that matter in early septic acute kidney injury: an experimental study 1 2 2 2 2 2 2* Jan Benes , Jiri Chvojka , Roman Sykora , Jaroslav Radej , Ales Krouzecky , Ivan Novak and Martin Matejovic Abstract Introduction: In almost half of all sepsis patients, acute kidney injury (AKI) develops. However, the pathobiologic differences between sepsis patients with and without AKI are only poorly understood. We used a unique opportunity to examine dynamic inflammatory, renal hemodynamic, and microvascular changes in two clinically relevant large-animal models of sepsis. Our aim was to assess variability in renal responses to sepsis and to identify both hemodynamic and nonhemodynamic mechanisms discriminating individuals with AKI from those in whom AKI did not develop. Methods: Thirty-six pigs were anesthetized, mechanically ventilated, and instrumented. After a recovery period, progressive sepsis was induced either by peritonitis (n = 13) or by continuous intravenous infusion of live Pseudomonas aeruginosa (n = 15). Eight sham operated-on animals served as time-matched controls. All animals received standard intensive care unit (ICU) care, including goal-directed hemodynamic management. Before, and at 12, 18, and 22 hours of sepsis, systemic and renal (ultrasound flow probe) hemodynamics, renal cortex microcirculation (laser Doppler), inflammation (interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-a), oxidative stress (thiobarbituric acid reactive species (TBARS), nitrite/nitrate concentrations (NOx), and renal oxygen kinetics and energy metabolism were measured.