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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 PMID25317032show 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/mm2, 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/mm2, p?0.001).We conclude that edaravone injected at the start of reperfusion can suppress not only muscle reperfusion injury but also lung damage.