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2014 ; 23
(3
): 193-6
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Edaravone injected at the start of reperfusion suppresses myonephropathic
metabolic syndrome in rats
#MMPMID25317032
Yamamura M
; Miyamoto Y
; Mitsuno M
; Tanaka H
; Ryomoto M
Int J Angiol
2014[Sep]; 23
(3
): 193-6
PMID25317032
show ga
The purpose of this study was to evaluate whether edaravone (Radicut(®),
Mitsubishi Tanabe Pharma Co., Osaka, Japan) injected at the start of reperfusion
can suppress myonephropathic-metabolic syndrome (MNMS). MNMS models were made by
clamping the bilateral common femoral arteries for 5 hours. At de-clamping (at
the start of reperfusion), they were intra-peritoneal injected with 9.0 mg/kg of
edaravone (the edaravone group, n?=?5) or an equal volume of saline (the control
group, n?=?5). At five hours after de-clamping, the lower extremity muscles were
stained with hematoxylin & eosin (H&E) to count the viable cells, and periodic
acid- Schiff (PAS) to assess the glycogen storage. The lungs were also stained
with H&E to expresse the alveolar wall thickness, and naphthol AS-D chloroacetate
esterase to label infiltrating active neutrophils. The viable muscle cells in the
edaravone group was significantly greater than that of the control group
(593?±?60 vs. 258?±?31 cells/mm(2), p?0.01). The PAS-positive area in the
edaravone group was also significantly higher than that in the control group
(30.1?±?6.9 vs. 7.3?±?2.1%, p?0.001). The alveolar wall thickness in the
edaravone group was significantly lower than that in the control group
(63.6?±?5.6 vs. 17.2?±?5.2%, p?0.001). The active neutrophil infiltration in
the edaravone group was also significantly lower than that in the control group
(249?±?59 vs. 68?±?8 cells/mm(2), p?0.001). We conclude that edaravone injected
at the start of reperfusion can suppress not only muscle reperfusion injury but
also lung damage.