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Ideal Size Range for Embolic Agents in Interventional Oncology Experiments Involving Rat Models of Hepatocellular Carcinoma
Affiliation:1. Department of Radiology, Asan Medical Center, Seoul, Korea;2. Department of Radiology, Seoul National University Hospital, Seoul, Korea;3. Department of Radiology, Seoul National University College of Medicine, Seoul, Korea
Abstract:PurposeTo optimize future translational research, this study aimed to determine the ideal range of sizes for embolic agents in interventional oncology experiments utilizing rat models of hepatocellular carcinoma (HCC).Materials and MethodsFifty-five male Sprague-Dawley rats were divided into 2 groups to evaluate the distribution of microparticles and tumor response rates. After implanting hepatoma cells into the rodent liver, fluorescent microparticles of sizes ranging from 5 to 35 μm were administered via the hepatic artery. In the first group, the distribution of microparticles was evaluated in hepatoma-free rats, and the tumor necrosis rates following administration of a predetermined aliquot of microparticles (0.4 mL) were measured in tumor-bearing rats. Thereafter, the 3 microparticle sizes associated with the best tumor response rates were chosen for analysis of the tumor necrosis rates following hepatic artery embolization until angiographic stasis is achieved in the second group.ResultsThe tendency for microparticles to distribute in nontarget organs increased as the microparticle size decreased below 15 μm. Tumor necrosis rates tended to be higher in rats treated with 15–19-μm microparticles than in those treated with 19–24-μm or 19–24-μm microparticles. The in-group deviation of the tumor necrosis rates was highest for microparticle sizes of 19–24 and 25–35 μm, which implies the proximal embolization of the hepatic artery for larger microparticle sizes. However, there was no statistical significance among the 3 groups (P = .095).ConclusionsThe 15–19-μm embolic agents were the most favorable for causing tumor necrosis without nontarget toxicity in the transarterial treatments of rat HCC models.
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