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Our study focused on the spatiotemporal analysis of reactive oxygen species (ROS), a key factor in hepatic ischemia-reperfusion injury, using a rat model to evaluate potential clinical applications. By inducing partial hepatic ischemia-reperfusion in rats through ligation of left portal vein and hepatic artery (one hour ischemia followed by reperfusion), we explored ROS generation using an imaging probe, 1-acetoxy-3-carbamoyl-2,2,5,5-tetramethylpyrroline (ACP), which reacts with ROS to produce a detectable T1-enhanced magnet resonance imaging (MRI) signal. In the rat model, the region of the left liver ischemia-reperfusion showed extremely mild liver injury one hour after reperfusion. After 12 h of reperfusion, extensive hepatocellular necrosis was observed, mainly in the hepatic interlobular region. One hour after reperfusion, the ACP-derived MRI signal increased in the region of left lobe ischemia-reperfusion was significantly higher than that in the non-ischemia-reperfusion region of the same rat right lobe. Administration of edaravone targeting the period of excessive ROS production at 1 h after reperfusion significantly suppressed hepatic injury 12 h after ischemia-reperfusion. Given MRI's crucial role in clinical diagnostics and its adaptability, our research suggests a promising strategy for early intervention in organ damage by monitoring and modulating ROS levels, potentially revolutionizing patient care.
Yamashita et al. (Thu,) studied this question.