PURPOSE: Free radicals have been implicated in myonephropathic metabolic syndrome (MNMS), which not only damages muscles but also the kidneys and lungs. It was recently shown that the free radical scavenger edaravone suppressed reperfusion injury in rat extremities. The present study evaluated whether edaravone also protects against MNMS-induced tissue damage in the lungs and kidneys after reperfusion injury of rat extremities. METHODS: Ten male Lewis rats (mean [± SD] weight 508±33 g) were divided into two groups. The MNMS models were created by clamping the bilateral common femoral arteries for 5 h, followed by declamping. In another group, 3.0 mg/kg of edaravone was injected into the peritoneal cavity before clamping the bilateral common femoral arteries. Five hours after starting reperfusion, the kidneys and lungs were harvested from each rat for histological study (n=10). Kidney damage was expressed as the number of infiltrating cells in the glomeruli. Lung damage was expressed as the percentage area of the alveolar wall thickness with cellular infiltration, using computerized densitometry. RESULTS: Kidneys in the edaravone group showed less cellular infiltration than in the control group (62.2±2.4 cells versus 75.8±3.6 cells per glomerulus, respectively; P=0.002). Lungs in the edaravone group also showed a significantly lower percentage of damaged lung tissue area than in the control group (20.5±1.5% versus 63.6±2.8%, respectively; P<0.001). CONCLUSION: The results suggest that the free radical scavenger edaravone might protect against kidney and lung damage induced by MNMS after reperfusion injury of rat extremities.
PURPOSE:Free radicals have been implicated in myonephropathic metabolic syndrome (MNMS), which not only damages muscles but also the kidneys and lungs. It was recently shown that the free radical scavenger edaravone suppressed reperfusion injury in rat extremities. The present study evaluated whether edaravone also protects against MNMS-induced tissue damage in the lungs and kidneys after reperfusion injury of rat extremities. METHODS: Ten male Lewis rats (mean [± SD] weight 508±33 g) were divided into two groups. The MNMS models were created by clamping the bilateral common femoral arteries for 5 h, followed by declamping. In another group, 3.0 mg/kg of edaravone was injected into the peritoneal cavity before clamping the bilateral common femoral arteries. Five hours after starting reperfusion, the kidneys and lungs were harvested from each rat for histological study (n=10). Kidney damage was expressed as the number of infiltrating cells in the glomeruli. Lung damage was expressed as the percentage area of the alveolar wall thickness with cellular infiltration, using computerized densitometry. RESULTS: Kidneys in the edaravone group showed less cellular infiltration than in the control group (62.2±2.4 cells versus 75.8±3.6 cells per glomerulus, respectively; P=0.002). Lungs in the edaravone group also showed a significantly lower percentage of damaged lung tissue area than in the control group (20.5±1.5% versus 63.6±2.8%, respectively; P<0.001). CONCLUSION: The results suggest that the free radical scavenger edaravone might protect against kidney and lung damage induced by MNMS after reperfusion injury of rat extremities.