Cotterill L A, Gower J D, Fuller B J, Green C J
Section of Surgical Research, Northwick Park Hospital, Harrow, Middlesex.
Transplantation. 1989 Nov;48(5):745-51. doi: 10.1097/00007890-198911000-00004.
Storage of rabbit kidneys at 0 degrees C for periods of 72 hr after flushing with hypertonic citrate solution, or 24 hr when flushed with isotonic saline, resulted in significant increases in Schiff base and thiobarbituric acid-reactive markers of lipid peroxidation in vitro. The extent of lipid peroxidation was not significantly altered by addition of verapamil (100 microM), a Ca++ channel blocking agent, or calcium 1 mM (CaCl2) to the HCA storage solution. In contrast, verapamil significantly reduced the extent of lipid peroxidation in kidneys stored in saline solution, and a significant increase in oxidative damage occurred when CaCl2 was added to this storage solution. Thus the extent of lipid peroxidation in kidneys stored in saline was significantly mediated by extracellular Ca++, whereas in HCA this was probably chelated by the large excess of citrate (55 mM) in this medium that prevented, or at least slowed, its entry into the renal cells. Lipid peroxidation was however significantly increased in kidneys stored in both HCA and saline solutions by addition of the calcium ionophore A23187 (10 microM) or the polysaccharide dye ruthenium red (5 microM) that inhibits mitochondrial uptake of Ca++. This strongly suggested that altered intracellular Ca++ homeostasis during the storage period played an important role in the development of oxidative damage to kidneys stored in both these media.
用高渗柠檬酸盐溶液冲洗后，兔肾在0摄氏度下保存72小时，或用等渗盐水冲洗后保存24小时，体外脂质过氧化的席夫碱和硫代巴比妥酸反应性标志物显著增加。向高渗柠檬酸盐溶液（HCA）储存液中添加维拉帕米（100微摩尔）（一种钙离子通道阻滞剂）或1毫摩尔钙（氯化钙），脂质过氧化程度没有显著改变。相比之下，维拉帕米显著降低了储存在盐溶液中的肾脏的脂质过氧化程度，而向该储存液中添加氯化钙时，氧化损伤显著增加。因此，储存在盐溶液中的肾脏的脂质过氧化程度明显由细胞外钙离子介导，而在HCA中，这可能被该培养基中大量过量的柠檬酸盐（55毫摩尔）螯合，从而阻止或至少减缓了其进入肾细胞。然而，通过添加钙离子载体A23187（10微摩尔）或抑制线粒体钙摄取的多糖染料钌红（5微摩尔），储存在HCA和盐溶液中的肾脏的脂质过氧化均显著增加。这有力地表明，储存期间细胞内钙离子稳态的改变在这两种培养基中储存的肾脏氧化损伤的发展中起重要作用。
