Protease-activated receptor 2 blocking peptide counteracts endotoxin-induced inflammation and coagulation and ameliorates glomerular fibrin deposition in a rat model of acute renal failure 英文参考文献.docVIP
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Protease-activated receptor 2 blocking peptide counteracts endotoxin-induced inflammation and coagulation and ameliorates glomerular fibrin deposition in a rat model of acute renal failure 英文参考文献
Available online /supplements/11/S4
Critical Care Volume 11 Suppl 4, 2007
Sepsis 2007
Paris, France, 26–29 September 2007
Published online: 26 September 2007
These abstracts are available online at /supplements/11/S4
? 2007 BioMed Central Ltd
P1
were performed with cytokine knockout mice, mice treated with
low-dose LPS (1, 5 mg/kg) as a sepsis model without induction of
hypotension, glucocorticoid-treated mice, and mice with renal
artery clipping serving as a model for renal ischemia.
Cytokine-mediated regulation of renal urea transporters
during sepsis
Christoph Schmidt, Klaus Hoecherl, Michael Bucher
Anaesthesiology Department, Hospital of the University of
Regensburg, Regensburg, Germany
Results and discussion LPS-injected mice (10 mg/kg) presented
with reduced glomerular filtration rate, fractional urea excretion and
inner medulla osmolality associated with a marked decrease in
expression of UT-A1, UT-A2, UT-A3, UT-A4 and UT-B (Figure 1).
Similar alterations were observed after application of TNFα, IL-1β,
IFNγ or IL-6. LPS-induced downregulation of urea transporters was
not affected in knockout mice with deficient TNFα, IL-receptor-1,
IFNγ or IL-6. Glucocorticoid treatment inhibited LPS-induced
increases of tissue TNFα, IL-1β, IFNγ or IL-6 concentration,
diminished LPS-induced renal dysfunction and attenuated the
downregulation of renal urea transporters. Injection of low-dose
LPS (1, 5 mg/kg) also led to renal dysfunction paralleled by a
downregulation of renal urea transporters without alterations in
blood pressure. Renal ischemia induced by renal artery clipping
did not influence the expression of urea transporters.
Critical Care 2007, 11(Suppl 4):P1 (doi: 10.1186/cc5980)
Background The pathogenesis of endotoxemic tubular dys-
function with failure in urine concentration is poorly understood.
Urea
plays an important role in the urinary co
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