Le Couteur D G, Rivory L P, Pond S M
University of Queensland Department of Medicine, Brisbane, Australia.
J Gastroenterol Hepatol. 1994 Jul-Aug;9(4):385-90. doi: 10.1111/j.1440-1746.1994.tb01260.x.
During liver transplantation, oxidative stress occurs during hypoxia and reoxygenation of the donor organ. Chemical oxidative stress impairs cell membrane transport. Therefore, in this study the influence of hypoxia and reoxygenation on hepatocellular membrane transport was investigated. Specifically, glucose transport was studied in the perfused rat liver using the multiple indicator-dilution technique. First, it was observed that in normal rat livers, glucose transport was rapid but saturable (Km 48 +/- 10 mmol/L and Vmax 9.4 +/- 0.9 mumol/s per g of liver). To stimulate hypoxia and reoxygenation, livers were perfused for 30 min with nitrogen-saturated buffer and then with oxygen-saturated buffer for 20 min. The livers from fed rats were protected from hypoxia-reoxygenation injury whereas those from fasted rats were highly susceptible to injury as determined by lactate dehydrogenase release. After reoxygenation, the rate of glucose influx decreased significantly by approximately 50% in the fasted livers (P < 0.001) but was unaffected in the fed livers. This impairment of the hepatocellular transport of glucose, which could be secondary to oxidative injury to the hepatocyte membrane, has implications for the function of donor livers that have sustained hypoxia-reoxygenation ('preservation') injury during transplantation.
在肝移植过程中，供体器官在缺氧和复氧期间会发生氧化应激。化学性氧化应激会损害细胞膜转运。因此，在本研究中，研究了缺氧和复氧对肝细胞膜转运的影响。具体而言，使用多指示剂稀释技术在灌注的大鼠肝脏中研究了葡萄糖转运。首先，观察到在正常大鼠肝脏中，葡萄糖转运迅速但具有饱和性（Km为48±10 mmol/L，Vmax为每克肝脏9.4±0.9 μmol/s）。为了模拟缺氧和复氧，肝脏先用氮气饱和缓冲液灌注30分钟，然后用氧气饱和缓冲液灌注20分钟。通过乳酸脱氢酶释放测定，喂食大鼠的肝脏对缺氧-复氧损伤具有抵抗力，而禁食大鼠的肝脏则极易受到损伤。复氧后，禁食肝脏中葡萄糖流入速率显著降低约50%（P<0.001），而喂食肝脏中则不受影响。这种肝细胞葡萄糖转运的损害可能继发于肝细胞膜的氧化损伤，这对在移植过程中遭受缺氧-复氧（“保存”）损伤的供体肝脏功能具有影响。
