严重烫伤大鼠延迟复苏后多器官损伤机制中的氧自由基作用

Multiple organ injury after delayed fluid resuscitation in severely scalded rats:role of oxygen free radicals

将66只悉生大鼠分为伤前对照组、早期复苏组、延迟复苏组和治疗组,采用ESR技术结合传统间接检测手段,观察了伤后8、24、48及72 h心、肝、肾及肺组织中的氧自由基(OFR)含量变化,同时还对脏器病理形态、动脉血气和血清肌酸磷酸激酶(CPK)、乳酸脱氧酶(LDH)、ALT(曾用GPT)、AST(曾用GOT)、BUN和肌酐(Cr)含量进行了观察。结果表明,早期复苏组和延迟复苏组各脏器均有OFR含量增加,同时均发生了病理形态学改变和动脉血气、血清学指标的异常,且延迟组的上述改变明显重于早期组,经抗氧化剂治疗后改善。提示延迟复苏是脏器OFR产生的重要促进因素。

Sixty gnotobiotic rats with 5 strains of bacteria in intestine were random- ized to 4 groups:Sham injury group(controls,n=6).Early fluid resuscitation (EFR)group(n=24),receiving fluid resuscitation(Parkland formula)immediatelly af- ter scald(40% TBSA,third degree).Delayed fluid resuscitation(DFR)group(n= 24)receiving resuscitation 6 hours later after scald.Treatment group(n=12)receiv- ing DFR and the therapy of VitC and VitE.At 8,24,48 and 72 hours after injury,the animals(n=6,at each point)were sacrificed and the content of oxygen free radicals (OFR),SOD,GSHPx and MDA in the heart,liver,kidney and lung were determined. Morphological Changes of organs,PaO_2,PaCO_2 and the content of serum CPK,LDH, GPT,GOT,BUN and Cr were also examined.Both EFR and DFR groups demonstrated elevated content of OFR and MDA and reduced content of SOD and GSHPx in their or- gans.Morphological and serological changes were also observed.All these changes were more obvious in DFR group than in EFR group.After the treatment of VitC and VitE, the changes were ameliorated.Our results suggested that DFR induced the production of OFR,resulting in lipid peroxidation and that OFR injury might be one of the main fac- tors in the pathogenesis of multiple organ injury after DFR.