Abstract 264: Edaravone Injected at the Start of Reperfusion Suppresses Lung Damage Caused by Myonephropathic Metabolic Syndrome in Rats
Introduction & Hypothesis Free radicals have been implicated in myonephropathic metabolic syndrome (MNMS), which damages not only muscles but also lungs. At ATVB 2012, we previously reported that radical scavenger, edaravone (Radicut®, Mitsubishi Tanabe Pharma Co., Japan) injected at the start of reperfusion suppresses muscle injury following leg ischemia in rats. In this study, we evaluated whether edaravone can suppress MNMS-induced lung damage following leg ischemia, if injected at the start of reperfusion.
Methods The MNMS models (Male Lewis rats, 525 ± 78 g, n = 10) were induced, by clamping the bilateral common femoral arteries for 5 hours and then de-clamping. The rats were intraperitoneally injected with either 9.0 mg / kg of edaravone (edaravone group; n = 5), or saline (MNMS group; n = 5) at the same time as de-clamping, corresponding to the start of reperfusion. Five hours after de-clamping, the both lungs were harvested and stained with hematoxylin & eosin (HE). Normal lungs without reperfusion were also harvested as control (n = 3). Lung damage was expressed as the percentage area of the alveolar wall thickness, determined by computerized densitometry (NIH Image Program J, Ver. 1.37).
Results The lungs of MNMS group had extensive swelling. But the lungs of the edaravone group were filled with air, similar to that of normal lungs (Figure attached, original 200x). The mean percentage area in the edaravone group was significantly lower than that in MNMS group (17.2 ± 5.2 vs. 63.6 ± 5.6%, p < 0.001).
Conclusions Our results suggest that edaravone injected at the start of reperfusion can suppress MNMS-induced lung damage following leg ischemia in rats.
- © 2013 by American Heart Association, Inc.