OBJECTIVE: In order to understand the characterization and evolution of pulmonary injury, a portal hypertension rat model was used to imitate the anhepatic phase during standard orthotopic liver transplantation without veno-venous bypass. METHODS: In this study, 135 healthy male Wistar rats were selected; in which 15 rats were assigned in the normal control (NC) group and the remaining 120 rats were used to establish a recoverable prehepatic portal hypertension model, which were further evenly divided into eight groups after ischemia-reperfusion: portal hypertensive control group (PHTC), R0h, R6h, R12h, R24h, R48h, R72h, and R7d groups. Meanwhile, arterial blood pressure, dry-to-wet weight ratios of the lung, alanine aminotransferase (ALT) level in serum, arterial oxygen pressure (PaO2), and myeloperoxidase (MPO) activity in lung tissue were measured. Morphology changes of the lung were observed using an optical microscope and a transmission electron microscope. RESULTS: The portal hypertension rat model was successfully established three weeks after the first operation. These portal hypertensive rats could withstand 1 hour at the anhepatic phase. Pulmonary injury severity increased to the most at 12-24 hours, and decreased to normal at seven days after reperfusion. CONCLUSION: Ischemia-reperfusion injury is an important mechanism that results in pulmonary injury after liver transplantation. It is safe for portal hypertensive rats to tolerate 1 hour at the anhepatic phase. Pulmonary injury was the most severe within 12-24 hours after ischemia-reperfusion.
OBJECTIVE: In order to understand the characterization and evolution of pulmonary injury, a portal hypertensionrat model was used to imitate the anhepatic phase during standard orthotopic liver transplantation without veno-venous bypass. METHODS: In this study, 135 healthy male Wistar rats were selected; in which 15 rats were assigned in the normal control (NC) group and the remaining 120 rats were used to establish a recoverable prehepatic portal hypertension model, which were further evenly divided into eight groups after ischemia-reperfusion: portal hypertensive control group (PHTC), R0h, R6h, R12h, R24h, R48h, R72h, and R7d groups. Meanwhile, arterial blood pressure, dry-to-wet weight ratios of the lung, alanine aminotransferase (ALT) level in serum, arterial oxygen pressure (PaO2), and myeloperoxidase (MPO) activity in lung tissue were measured. Morphology changes of the lung were observed using an optical microscope and a transmission electron microscope. RESULTS: The portal hypertensionrat model was successfully established three weeks after the first operation. These portal hypertensiverats could withstand 1 hour at the anhepatic phase. Pulmonary injury severity increased to the most at 12-24 hours, and decreased to normal at seven days after reperfusion. CONCLUSION:Ischemia-reperfusion injury is an important mechanism that results in pulmonary injury after liver transplantation. It is safe for portal hypertensiverats to tolerate 1 hour at the anhepatic phase. Pulmonary injury was the most severe within 12-24 hours after ischemia-reperfusion.