Marubayashi S, Dohi K, Yamada K, Kawasaki T
Department of Surgery, Hiroshima University School of Medicine, Japan.
Surgery. 1991 Sep;110(3):537-43.
This study was undertaken to determine whether hepatic ischemia and the subsequent reflow of blood have any effect on the conversion of xanthine dehydrogenase to xanthine oxidase (XO). Ischemia of the liver for 90 or 120 minutes did not permit survival of the animals. XO represented 15% of the total xanthine dehydrogenase plus XO activity in the control liver. XO activity remained unchanged even after 90 minutes of hepatic ischemia, although a marked increase in lipid peroxide in the liver tissue was observed during the reperfusion. When hepatic ischemia was prolonged for 6 hours (animals were dead), XO activity rose to 35% of the total activity. Incubation of the liver at 37 degrees C resulted in a definite change in XO activity dependent on the length of incubation period. Although no significant changes occurred in XO activity during the first 2 hours of incubation, a marked XO conversion was observed between 2 and 4 hours, and a maximal conversion was achieved after 6 hours of incubation. These results suggest that XO newly generated during ischemia has a very limited role in oxygen free radical production after resuming perfusion.
本研究旨在确定肝脏缺血及随后的血液再灌注是否对黄嘌呤脱氢酶向黄嘌呤氧化酶（XO）的转化有任何影响。肝脏缺血90或120分钟会导致动物无法存活。在对照肝脏中，XO占黄嘌呤脱氢酶与XO总活性的15%。即使肝脏缺血90分钟后，XO活性仍保持不变，尽管在再灌注期间观察到肝组织中的脂质过氧化物显著增加。当肝脏缺血延长至6小时（动物死亡）时，XO活性升至总活性的35%。在37℃孵育肝脏会导致XO活性根据孵育时间的长短发生明确变化。尽管在孵育的前2小时XO活性没有显著变化，但在2至4小时观察到明显的XO转化，孵育6小时后实现最大转化。这些结果表明，缺血期间新产生的XO在恢复灌注后产生氧自由基方面的作用非常有限。
