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目的：探讨小儿烫伤休克期复苏前后血清、创面水泡液SOD、LPO的改变。方法：选择30例严重烫伤病儿在复苏前后行血清和创面水泡液SOD、LPO检测。30例正常小儿血清SOD、LPO的含量为正常对照组。结果：烫伤组复苏前血清SOD、LPO接近正常对照组，复苏后血清SOD明显降低、LPO明显升高，两者和对照组及复苏前比较均有显著性差异（P均＜0．01）。水泡液复苏前SOD为57．88±23.11、LPO为0．64±0．27，复苏后水泡液SOD较复苏前明显降低（28.8±5．59、p＜0．01），LPO和复苏前无明显差异（0.69±0.21、P＞0．05）。结论：延迟复苏是脏器大量产生OFR的主要促进因素，即缺血再灌注损伤，创面水泡液在复苏前有保留价值。
Objective: To investigate the changes of SOD and LPO in serum and wound fluid before and after resuscitation in children with scald and shock. Methods: Thirty children with severe scald were selected to detect serum and wound vesicular fluid SOD and LPO before and after resuscitation. 30 cases of normal children serum SOD, LPO content of the normal control group. Results: Serum SOD and LPO in scalded group before resuscitation were similar to those in normal control group. Serum SOD decreased significantly and LPO increased significantly after resuscitation. There was significant difference between the two groups before and after resuscitation (P <0.01). The level of SOD in blister fluid before resuscitation was 57.88 ± 23.11 and the LPO was 0.64 ± 0.27. After resuscitation, the SOD in blister fluid was significantly lower than that before resuscitation (28.8 ± 5.59, p <0.01) No significant difference (0.69 ± 0.21, P> 0.05). CONCLUSION: Delayed resuscitation is the main factor contributing to the massive organogenesis of OFR in organ, ie, ischemia-reperfusion injury and the preservation of vesicular fluid before resuscitation.