@article{SchickBaarFlemmingetal.2014,
  author    = {Schick, Martin A. and Baar, Wolfgang and Flemming, Sven and Schlegel, Nicolas and Wollborn, Jakob and Held, Christopher and Schneider, Reinhard and Brock, Robert W. and Roewer, Norbert and Wunder, Christian},
  title     = {Sepsis-induced acute kidney injury by standardized colon ascendens stent peritonitis in rats - a simple, reproducible animal model},
  series = {Intensive Care Medicine Experimental},
  volume    = {2},
  journal   = {Intensive Care Medicine Experimental},
  number    = {34},
  doi       = {10.1186/s40635-014-0034-x},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-126111},
  year      = {2014},
  abstract  = {Background Up to 50\% of septic patients develop acute kidney injury (AKI). The pathomechanism of septic AKI is poorly understood. Therefore, we established an innovative rodent model to characterize sepsis-induced AKI by standardized colon ascendens stent peritonitis (sCASP). The model has a standardized focus of infection, an intensive care set up with monitoring of haemodynamics and oxygenation resulting in predictable impairment of renal function, AKI parameters as well as histopathology scoring. Methods Anaesthetized rats underwent the sCASP procedure, whereas sham animals were sham operated and control animals were just monitored invasively. Haemodynamic variables and blood gases were continuously measured. After 24 h, animals were reanesthetized; cardiac output (CO), inulin and PAH clearances were measured and later on kidneys were harvested; and creatinine, urea, cystatin C and neutrophil gelatinase-associated lipocalin (NGAL) were analysed. Additional sCASP-treated animals were investigated after 3 and 9 days. Results All sCASP-treated animals survived, whilst ubiquitous peritonitis and significantly deteriorated clinical and macrohaemodynamic sepsis signs after 24 h (MAP, CO, heart rate) were obvious. Blood analyses showed increased lactate and IL-6 levels as well as leucopenia. Urine output, inulin and PAH clearance were significantly decreased in sCASP compared to sham and control. Additionally, significant increase in cystatin C and NGAL was detected. Standard parameters like serum creatinine and urea were elevated and sCASP-induced sepsis increased significantly in a time-dependent manner. The renal histopathological score of sCASP-treated animals deteriorated after 3 and 9 days. Conclusions The presented sCASP method is a standardized, reliable and reproducible method to induce septic AKI. The intensive care set up, continuous macrohaemodynamic and gas exchange monitoring, low mortality rate as well as the opportunity of detailed analyses of kidney function and impairments are advantages of this setup. Thus, our described method may serve as a new standard for experimental investigations of septic AKI.},
  language  = {en}
}
@article{EnigkWagnerSamapatietal.2014,
  author    = {Enigk, Fabian and Wagner, Antje and Samapati, Rudi and Rittner, Heike and Brack, Alexander and Mousa, Shaaban A. and Sch{\"a}fer, Michael and Habazettl, Helmut and Sch{\"a}per, J{\"o}rn},
  title     = {Thoracic epidural anesthesia decreases endotoxin-induced endothelial injury},
  series = {BMC Anesthesiology},
  volume    = {14},
  journal   = {BMC Anesthesiology},
  number    = {23},
  doi       = {10.1186/1471-2253-14-23},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-116787},
  year      = {2014},
  abstract  = {Background: The sympathetic nervous system is considered to modulate the endotoxin-induced activation of immune cells. Here we investigate whether thoracic epidural anesthesia with its regional symapathetic blocking effect alters endotoxin-induced leukocyte-endothelium activation and interaction with subsequent endothelial injury. Methods: Sprague Dawley rats were anesthetized, cannulated and hemodynamically monitored. E. coli lipopolysaccharide (Serotype 0127: B8, 1.5 mg x kg(-1) x h(-1)) or isotonic saline (controls) was infused for 300 minutes. An epidural catheter was inserted for continuous application of lidocaine or normal saline in endotoxemic animals and saline in controls. After 300 minutes we measured catecholamine and cytokine plasma concentrations, adhesion molecule expression, leukocyte adhesion, and intestinal tissue edema. Results: In endotoxemic animals with epidural saline, LPS significantly increased the interleukin-1 beta plasma concentration (48\%), the expression of endothelial adhesion molecules E-selectin (34\%) and ICAM-1 (42\%), and the number of adherent leukocytes (40\%) with an increase in intestinal myeloperoxidase activity (26\%) and tissue edema (75\%) when compared to healthy controls. In endotoxemic animals with epidural infusion of lidocaine the values were similar to those in control animals, while epinephrine plasma concentration was 32\% lower compared to endotoxemic animals with epidural saline. Conclusions: Thoracic epidural anesthesia attenuated the endotoxin-induced increase of IL-1 beta concentration, adhesion molecule expression and leukocyte-adhesion with subsequent endothelial injury. A potential mechanism is the reduction in the plasma concentration of epinephrine.},
  language  = {en}
}