Werker P M, Kon M, Green C J, Ambrose I, Hildago A
Department of Plastic, Reconstructive and Hand Surgery, University Hospital Utrecht, The Netherlands.
Br J Plast Surg. 1995 Dec;48(8):590-6. doi: 10.1016/0007-1226(95)90050-0.
An in vitro lipid peroxidation study measuring Schiff base and TBAR formation in homogenates of the fat and skin fractions of epigastric free flaps of DA-rats was performed to determine the role of oxygen-derived free radicals (ODFRs) in the aetiology of ischaemic injury and of ischaemia and reperfusion injury following cold (0-1 degree C) storage. The storage intervals were 0, 48, 72, 96 and 120 h in the study on ischaemic injury and 72 and 96 h in the study on combined ischaemia and reperfusion injury. Reperfusion was accomplished by anastomosing the pedicle vessels of the flap to the femoral vessels of a recipient; the reperfusion period was 15 min. In addition to a control group (C), three experimental groups were created to test the benefit of a preischaemic single passage perfusion with a hypertonic citrate solution (HCA), a pre- and postischaemic treatment with desferrioxamine (DFX) and a pre- and postischaemic treatment with lipoic acid (LA). The susceptibility of homogenates of skin and fat fractions of epigastric free flaps in DA-rats for lipid peroxidation increased significantly whenever the cold (0-1 degree C) ischaemic interval was prolonged from 0 to 72 h. These findings offer circumstantial evidence for the role of ODFRs in the aetiology of ischaemic injury. Following a short reperfusion period after extended periods of cold (0-1 degree C) ischaemia, no significant increase in susceptibility for lipid peroxidation could be found. Furthermore, no unequivocal role in the prevention of ischaemia and/or reperfusion injury by the use of either HCA, or DFX or LA could be found. The exact role of ODFRs in the aetiology of ischaemia-reperfusion injury in this setting remains unclear.
进行了一项体外脂质过氧化研究，测量DA大鼠上腹部游离皮瓣脂肪和皮肤部分匀浆中席夫碱和硫代巴比妥酸反应物（TBAR）的形成，以确定氧衍生自由基（ODFRs）在缺血性损伤以及冷（0-1摄氏度）储存后的缺血再灌注损伤病因中的作用。在缺血性损伤研究中，储存间隔为0、48、72、96和120小时，在缺血再灌注联合损伤研究中为72和96小时。通过将皮瓣的蒂血管与受体的股血管吻合来实现再灌注；再灌注期为15分钟。除了对照组（C）外，还设立了三个实验组，以测试缺血前单次通过高渗柠檬酸盐溶液（HCA）灌注、去铁胺（DFX）的缺血前后治疗以及硫辛酸（LA）的缺血前后治疗的益处。当冷（0-1摄氏度）缺血间隔从0延长至72小时时，DA大鼠上腹部游离皮瓣皮肤和脂肪部分匀浆对脂质过氧化的敏感性显著增加。这些发现为ODFRs在缺血性损伤病因中的作用提供了间接证据。在长时间冷（0-1摄氏度）缺血后的短时间再灌注期后，未发现脂质过氧化敏感性有显著增加。此外，未发现使用HCA、DFX或LA在预防缺血和/或再灌注损伤方面有明确作用。在这种情况下，ODFRs在缺血再灌注损伤病因中的确切作用仍不清楚。
