Hamamoto I, Nemoto E M, Evans R W, Mischinger H J, Fujita S, Murase N, Todo S
Department of Surgery, University of Pittsburgh School of Medicine, Pennsylvania 15261.
J Surg Res. 1993 Oct;55(4):382-9. doi: 10.1006/jsre.1993.1157.
Rat livers were flushed and stored ex vivo in Krebs-Henseleit buffer at 37 degrees C for 3 hr or in University of Wisconsin solution at 2 degrees C for 48 hr. After this they were perfused with recirculated Krebs-Henseleit solution at 37 degrees C for 1 hr. Levels of phospholipids (PL), free fatty acids (FFA), and conjugated dienes were determined at various times during ischemia and after 1 hr of reperfusion. After 3 hr warm ischemia, total PL content decreased by about 30% primarily because of decreases in phosphatidylcholine and phosphatidylethanolamine. One hour of reperfusion normalized PL levels. Total PL content was unchanged up to 48 hr of cold ischemia because of offsetting alterations in levels of PL classes. FFA accumulation during warm ischemia was about half that during cold ischemia. Conjugated diene concentration increased fivefold during warm ischemia but was unchanged during cold ischemia. Low PL levels and FFA accumulation along with production of conjugated dienes suggest that lipid oxidation is a major mechanism of PL degradation during warm, but not cold, ischemia of the liver.
将大鼠肝脏冲洗后,在37℃的Krebs-Henseleit缓冲液中离体保存3小时,或在2℃的威斯康星大学溶液中保存48小时。之后,在37℃用循环的Krebs-Henseleit溶液灌注1小时。在缺血期间的不同时间点以及再灌注1小时后,测定磷脂(PL)、游离脂肪酸(FFA)和共轭二烯的水平。热缺血3小时后,总PL含量下降约30%,主要是由于磷脂酰胆碱和磷脂酰乙醇胺含量降低。再灌注1小时后,PL水平恢复正常。由于PL类别水平的变化相互抵消,冷缺血48小时内总PL含量无变化。热缺血期间FFA的积累约为冷缺血期间的一半。共轭二烯浓度在热缺血期间增加了五倍,但在冷缺血期间没有变化。低PL水平、FFA积累以及共轭二烯的产生表明,脂质氧化是肝脏热缺血而非冷缺血期间PL降解的主要机制。