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2017 ; 50
(1
): 11-19
Nephropedia Template TP
gab.com Text
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English Wikipedia
Histological and Immunohistochemical Basis of the Effect of Aminoguanidine on
Renal Changes Associated with Hemorrhagic Shock in a Rat Model
#MMPMID28386146
Al Drees A
; Salah Khalil M
; Soliman M
Acta Histochem Cytochem
2017[Feb]; 50
(1
): 11-19
PMID28386146
show ga
Acute kidney failure is the main cause of death among patients with severe trauma
due to massive blood loss and hemorrhagic shock (HS). Renal cell injury is caused
by tissue ischemia. Renal ischemia initiates a complex and interconnected chain
of events resulting in cell injury and renal cell necrosis. Nitric oxide plays a
crucial role in renal function and can be inhibited by aminoguanidine (AG). We
studied whether AG can ameliorate pathological renal changes associated with HS
syndrome in a rat model and explored the AG protection mechanism. Rats were
intraperitoneally injected with heparin sodium and mean arterial blood pressure
was monitored. Animals were divided into three groups: control (without
hemorrhage), with or without intra-arterially injected AG; HS (blood continuously
withdrawn or reinfused to maintain an MABP of 35-40 mmHg); and HS with AG. We
found that AG decreased plasma concentrations of urea, creatinine, and nitrates;
ameliorated histological changes of HS-induced rats; and decreased the
expressions of inducible nitrogen oxide synthase (iNOS), proapoptotic protein
(BAX), and vitamin D receptors (VDR). AG ameliorated kidney injury by inhibiting
iNOS resulting in decreased BAX and VDR expressions. Therefore, a therapeutic
strategy targeting AG may provide new insights into kidney injury during severe
shock.