Experimental and clinical transplantation : official journal of the Middle East Society for Organ Transplantation · 2026
Experimental Hepatic Ischemia-Reperfusion Injury Model in Rats: the Optimum Ischemia and Reperfusion Durations.
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Fakıoğlu Ender, Bilgili Gamze, Özdemir Binnaz Handan, Yavuz Çolak Meriç, Güney Lütfi Hakan, Karakaya Emre, Yalçın Yaprak, Baysan Çebi Pınar, Ataç Fatma Belgin
Аннотация
OBJECTIVES: Hepatic ischemia-reperfusion injury is a major contributor to posttransplant liver graft dysfunction and postoperative complications. Although rat models are commonly used in hepatic ischemia-reperfusion injury research, standardized durations for ischemia and reperfusion remain undefined. Here, we aimed to identify optimal ischemia and reperfusion durations for a reliable and reproducible experimental hepatic ischemia-reperfusion injury model in rats.
MATERIALS AND METHODS: We randomly assigned 45 male Wistar rats into groups with 100% hepatic perfusion blockade for 45 or 90 minutes, followed by reperfusion periods of 3, 6, 12, 24, and 48 hours. We evaluated survival rates, histopathologic liver damage (Suzuki scoring) with neutrophilic infiltration, and biochemical parameters. We excluded rats that underwent 90 minutes of ischemia or >6 hours of reperfusion (which experienced high mortality) from further analyses.
RESULTS: The 45-minute ischemia/6-hour reperfusion group exhibited significant liver injury compared with the sham and 3-hour groups, with elevated serum alanine aminotransferase and aspartate ami-notransferase, reduced hepatic ATP, and increased levels of total oxidant status, myeloperoxidase, and tumor necrosis factor-α (P < .05). Histopathological findings confirmed higher vacuolization and neutrophilic infiltration in this group. Three-hour reperfusion yielded only mild elevations in myeloperoxidase and tumor necrosis factor-α without significant tissue injury.
CONCLUSIONS: The model of 45 minutes of ischemia followed by 6 hours of reperfusion reliably induced hepatic ischemia-reperfusion injury in rats, supported by both biochemical and histological parameters. This standardized model balances reproducibility and animal survivability, offering a robust foundation for future hepatic ischemia-reperfusion injury research.
MATERIALS AND METHODS: We randomly assigned 45 male Wistar rats into groups with 100% hepatic perfusion blockade for 45 or 90 minutes, followed by reperfusion periods of 3, 6, 12, 24, and 48 hours. We evaluated survival rates, histopathologic liver damage (Suzuki scoring) with neutrophilic infiltration, and biochemical parameters. We excluded rats that underwent 90 minutes of ischemia or >6 hours of reperfusion (which experienced high mortality) from further analyses.
RESULTS: The 45-minute ischemia/6-hour reperfusion group exhibited significant liver injury compared with the sham and 3-hour groups, with elevated serum alanine aminotransferase and aspartate ami-notransferase, reduced hepatic ATP, and increased levels of total oxidant status, myeloperoxidase, and tumor necrosis factor-α (P < .05). Histopathological findings confirmed higher vacuolization and neutrophilic infiltration in this group. Three-hour reperfusion yielded only mild elevations in myeloperoxidase and tumor necrosis factor-α without significant tissue injury.
CONCLUSIONS: The model of 45 minutes of ischemia followed by 6 hours of reperfusion reliably induced hepatic ischemia-reperfusion injury in rats, supported by both biochemical and histological parameters. This standardized model balances reproducibility and animal survivability, offering a robust foundation for future hepatic ischemia-reperfusion injury research.