手术时机对多发创伤后肝损害影响的实验研究
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摘要
目的：多发伤的治疗中常会涉及到肝缺血再灌注损伤,严重多发创伤后肝脏的缺血耐受性及手术时机的选择是不确定的,本实验观察多发骨折合并肝缺血再灌注损伤后肝缺血耐受性变化及不同骨折治疗时机对肝损害的影响。
方法：采取动物实验,第一部分：建立多发骨折合并肝缺血再灌注损伤模型,72只SD大鼠随机分成三组(每组18只),骨折(Fracture, F)组、肝缺血再灌注损伤(Hepatic Injury,HI)组、骨折+肝损伤(Fracture+ Hepatic Injury, F+HI)组。对照组为假手术(Sham)组(6只)。假手术组仅行腹部皮肤切开并缝合皮肤：骨折组应用自制双股骨骨折造模支架致双侧股骨干骨折；肝损伤组行剖腹血管夹夹闭肝蒂30分钟后再灌注造成肝缺血再灌注损伤；骨折+肝损伤组为多发骨折合并肝缺血再灌注损伤,模型制作完成后通过X线了解骨折类型、移位情况,于造模成功后1、24、48、72h处死大鼠取肝脏应用PCR方法检测肝组织中TNF-a、IL-6、IL-10mRNA表达,髓过氧化物酶(MPO)含量,取腹主动脉血检测ALT、血乳酸水平,并行组织学检查肝脏损伤情况。第二部分：将32只雄性SD大鼠随机分成4组(每组动物各8只)：骨折早手术(Fracture Early Surgery, FES)组、骨折晚手术(Fracture Later Surgery, FLS)组、骨折+肝损伤早手术(Fracture+Hepatic Injury Early Surgery,, F+HIES)组、骨折+肝损伤晚手术(Fracture+Hepatic Injury Later Surgery, F+HILS)组。早期手术为伤后1h内骨折髓内钉治疗,晚期手术为损伤后先用夹板固定骨折端72h后骨折髓内钉治疗。骨折治疗完成后6h应用PCR方法检测肝组织中TNF-a、IL-6、IL-10mRNA表达,检测髓过氧化物酶(MPO)含量,取腹主动脉血检测谷丙转氨酶(ALT)、血乳酸(LD),肝组织常规固定,HE染色后光镜检查。
结果：第一部分：模型制作完成后行X线摄片证实双侧股骨干骨折均为闭合性中段横断骨折,骨折移位明显。骨折组、肝损伤组、骨折+肝损伤组大鼠血ALT、LD,肝脏MPO在1h升高,24h达到高峰,48h、72h下降,骨折+肝损伤组较骨折组、肝损伤组增高明显(P<0.05)。骨折组、肝损伤组、骨折+肝损伤组肝脏TNF-amRNA表达在1h升高,24h达到高峰,48h、72h下降；骨折+肝损伤组较骨折组、肝损伤组各个时间点均增高明显(P<0.05)；骨折组、肝损伤组、骨折+肝损伤组肝脏IL-6mRNA表达在1h、24h升高,48h达到高峰,72h下降。骨折+肝损伤组较骨折组、肝损伤组增高明显(P<0.05)；骨折组、肝损伤组、骨折+肝损伤组肝脏IL-10mRNA表达在1h、24h、48h升高,72h达到高峰。骨折+肝损伤组较骨折组、肝损伤组增高明显(P<0.05)三组大鼠肝脏病理切片显示肝窦充血、肝细胞肿胀、炎性细胞浸润,骨折+肝损伤组较其他两组肝细胞坏死、炎性细胞浸润显著。第二部分：骨折+肝损伤早手术组肝脏TNF-a、IL-6、IL-10mRNA表达含量、MPO含量、血ALT、血LD水平明显高于骨折早手术组、骨折晚手术组、骨折+肝损伤晚手术组(P<0.05)。骨折早手术组肝脏TNF-a、IL-6、IL-10mRNA表达含量、MPO含量、血ALT、血LD水平与骨折晚手术组比较差异较小。骨折+肝损伤早手术组肝脏充血、炎细胞浸润、细胞坏死等病理学改变显著。
结论：多发骨折合并肝缺血再灌注损伤后肝脏炎性改变及细胞坏死的病理学早期(1h)改变明显,后期(72h)肝耐受性增加。手术时机对多发骨折后肝损害影响小,多发骨折合并肝缺血再灌注损伤后早期骨折治疗导致肝损害加重,损伤控制治疗能增加肝脏对于创伤的耐受性,降低肝损害程度。
Objective:The managemengt of polytrauma frequently involves hepatic ischemia reperfusion injury。Hepatic ischemia tolerance and operation time selection after polytrauma are uncertain,the purpose of this experiment is to study that hepatic tolerance variation and deferent fracture management timing impact hepatic lesion after multiple fracture combining hepatic ischemia reperfusion injury。
Methods:Animal study,partⅠ:establish the animal model of multiple fracture combining hepatic ischemia reperfusion injury.。Seventy-two SD rats were randomly divided into there groups(18 for each group):Fracture (F)group、Hepatic Injury(HI)group、Fracture+Hepatic Injury (F+HI)group。Contrast group is Sham Operation(Sham)group(6 for this group)。Sham group,only abdominal skin incision and skin closure; Bilateral femoral shaft fractures were caused by self-made device in Fracture group; Hepatic ischemia reperfusion injury was caused by Vascular liver pedicle clamping clip after 30 minutes to relax blood vessels in Hepatic Injury group; Fracture+Hepatic Injury group was fracture combining hepatic injury。Type and displacement of fracture were examed by X-ray after model completed, The expression of tumor necrosis factor-a (TNF-a)、interleukin-6(IL-6)、interleukin-10(IL-10) of hepatic tissue were detected by reverse transcription polymerase chain reaction(RT-PCR) after 1、24、48、72h of fracture management, hepatic myeloperoxidase (MPO) were detected, The contents of serum alanine aminotransferase(ALT)、lactic acid (LD) from abdominal aorta were detected. The morphological changes were observed by hematoxylin and eosin(HE)staining. PartⅡ:Thirty two SD rats were randomly divided into four groups(8 for each group):Fracture Early Surgery(FES)group、Fracture later Surgery(FLS)group、Fracture+Hepatic Injury Early Surgery(F+HIES)group、Fracture+Hepatic Injury Later Surgery,(F+HILS) group。Early surgery defined as the intramedullary nail treatment of fracture after injury 1h, later surgery defined as splint fracture after injury and the intramedullary nail treatment of fracture after injury 72h。The expression of tumor necrosis factor-a (TNF-a)、interleukin-6(IL-6)、interleukin-10(IL-10) of hepatic tissue were detected by reverse transcription polymerase chain reaction(RT-PCR) after 6h of fracture management, hepatic myeloperoxidase (MPO) were detected, The contents of serum alanine aminotransferase(ALT)、lactic acid (LD) from abdominal aorta were detected。The morphological changes were observed by hematoxylin and eosin(HE)staining。
Result:PartⅠ:X-ray shows that bilateral femoral fractures were closed fractures and significant shaft after model completed。Serum ALT、LD、MPO of three groups elevated in 1h,reached a peak in 24h,down in 48h、72h,The contents of Serum ALT、LD、MPO were significantly higher of Fracture+Hepatic Injury group than Fracture group or Hepatic Injury group (P<0.05)。The expression of tumor necrosis factor-a (TNF-a)of fracture group、hepatic injury group and fracture+hepatic injury group elevated in 1h, reached a peak in 24h,down in 48h、72h, the expression of tumor necrosis factor-a (TNF-a) of Fracture+Hepatic Injury group group was significantly higher than Fracture group or Hepatic Injury group (P<0.05); The expression of interleukin-6(IL-6) of fracture group、hepatic injury group and fracture+hepatic injury group elevated in 1h, reached a peak in 24h,down in 48h、72h, the expression of interleukin-6(IL-6) of Fracture+Hepatic Injury group was significantly higher than Fracture group or Hepatic Injury group(P<0.05); The expression of interleukin-10(IL-10) of fracture group、hepatic injury group and fracture+hepatic injury group elevated in 1h、24h、48h, reached a peak in 72h, the expression of interleukin-10(IL-10) of Fracture+Hepatic Injury group was significantly higher than Fracture group or Hepatic Injury group (P<0.05)。Rat liver biopsy in three groups shows Sinusoidal congestion、liver cell swelling,、inflammatory cell infiltration, Liver cell necrosis, inflammatory cell infiltration significantly in Fracture+Hepatic Injury group。PartⅡ:The expression of tumor necrosis factor-a (TNF-a)、interleukin-6(IL-6)、interleukin-10(IL-10)and the contents of hepatic myeloperoxidase (MPO)、serum ALT、serum LD in F+HIES group were higher than FES group or FLS group or F+HILS group (P<0.05)。The expression of tumor necrosis factor-a (TNF-a)、interleukin-6(IL-6)、interleukin-10(IL-10) and the contents of hepatic myeloperoxidase (MPO)、serum ALT、serum LD in FES group were similar with FLS group。F+HIES group of liver congestion, inflammatory cell infiltration, cell necrosis and other pathological changes significant.
Conclusion:Liver cell necrosis, inflammatory changes、pathological changes and hepatic tolerence declining of the early stage (1h)was significantly after Multiple fractures complicated with hepatic ischemia-reperfusion injury. However, hepatic tolerance enhanced in later stage (72h)。Timing of surgery effect on liver lesion after multiple fractures is small, the early fracture treatment of multiple fractures complicated with hepatic ischemia-reperfusion injury can lead to that liver lesion aggravate, treatment of damage control can increase the hepatic tolerance for the trauma and decrease liver lesion。
方法：采取动物实验,第一部分：建立多发骨折合并肝缺血再灌注损伤模型,72只SD大鼠随机分成三组(每组18只),骨折(Fracture, F)组、肝缺血再灌注损伤(Hepatic Injury,HI)组、骨折+肝损伤(Fracture+ Hepatic Injury, F+HI)组。对照组为假手术(Sham)组(6只)。假手术组仅行腹部皮肤切开并缝合皮肤：骨折组应用自制双股骨骨折造模支架致双侧股骨干骨折；肝损伤组行剖腹血管夹夹闭肝蒂30分钟后再灌注造成肝缺血再灌注损伤；骨折+肝损伤组为多发骨折合并肝缺血再灌注损伤,模型制作完成后通过X线了解骨折类型、移位情况,于造模成功后1、24、48、72h处死大鼠取肝脏应用PCR方法检测肝组织中TNF-a、IL-6、IL-10mRNA表达,髓过氧化物酶(MPO)含量,取腹主动脉血检测ALT、血乳酸水平,并行组织学检查肝脏损伤情况。第二部分：将32只雄性SD大鼠随机分成4组(每组动物各8只)：骨折早手术(Fracture Early Surgery, FES)组、骨折晚手术(Fracture Later Surgery, FLS)组、骨折+肝损伤早手术(Fracture+Hepatic Injury Early Surgery,, F+HIES)组、骨折+肝损伤晚手术(Fracture+Hepatic Injury Later Surgery, F+HILS)组。早期手术为伤后1h内骨折髓内钉治疗,晚期手术为损伤后先用夹板固定骨折端72h后骨折髓内钉治疗。骨折治疗完成后6h应用PCR方法检测肝组织中TNF-a、IL-6、IL-10mRNA表达,检测髓过氧化物酶(MPO)含量,取腹主动脉血检测谷丙转氨酶(ALT)、血乳酸(LD),肝组织常规固定,HE染色后光镜检查。
结果：第一部分：模型制作完成后行X线摄片证实双侧股骨干骨折均为闭合性中段横断骨折,骨折移位明显。骨折组、肝损伤组、骨折+肝损伤组大鼠血ALT、LD,肝脏MPO在1h升高,24h达到高峰,48h、72h下降,骨折+肝损伤组较骨折组、肝损伤组增高明显(P<0.05)。骨折组、肝损伤组、骨折+肝损伤组肝脏TNF-amRNA表达在1h升高,24h达到高峰,48h、72h下降；骨折+肝损伤组较骨折组、肝损伤组各个时间点均增高明显(P<0.05)；骨折组、肝损伤组、骨折+肝损伤组肝脏IL-6mRNA表达在1h、24h升高,48h达到高峰,72h下降。骨折+肝损伤组较骨折组、肝损伤组增高明显(P<0.05)；骨折组、肝损伤组、骨折+肝损伤组肝脏IL-10mRNA表达在1h、24h、48h升高,72h达到高峰。骨折+肝损伤组较骨折组、肝损伤组增高明显(P<0.05)三组大鼠肝脏病理切片显示肝窦充血、肝细胞肿胀、炎性细胞浸润,骨折+肝损伤组较其他两组肝细胞坏死、炎性细胞浸润显著。第二部分：骨折+肝损伤早手术组肝脏TNF-a、IL-6、IL-10mRNA表达含量、MPO含量、血ALT、血LD水平明显高于骨折早手术组、骨折晚手术组、骨折+肝损伤晚手术组(P<0.05)。骨折早手术组肝脏TNF-a、IL-6、IL-10mRNA表达含量、MPO含量、血ALT、血LD水平与骨折晚手术组比较差异较小。骨折+肝损伤早手术组肝脏充血、炎细胞浸润、细胞坏死等病理学改变显著。
结论：多发骨折合并肝缺血再灌注损伤后肝脏炎性改变及细胞坏死的病理学早期(1h)改变明显,后期(72h)肝耐受性增加。手术时机对多发骨折后肝损害影响小,多发骨折合并肝缺血再灌注损伤后早期骨折治疗导致肝损害加重,损伤控制治疗能增加肝脏对于创伤的耐受性,降低肝损害程度。
Objective:The managemengt of polytrauma frequently involves hepatic ischemia reperfusion injury。Hepatic ischemia tolerance and operation time selection after polytrauma are uncertain,the purpose of this experiment is to study that hepatic tolerance variation and deferent fracture management timing impact hepatic lesion after multiple fracture combining hepatic ischemia reperfusion injury。
Methods:Animal study,partⅠ:establish the animal model of multiple fracture combining hepatic ischemia reperfusion injury.。Seventy-two SD rats were randomly divided into there groups(18 for each group):Fracture (F)group、Hepatic Injury(HI)group、Fracture+Hepatic Injury (F+HI)group。Contrast group is Sham Operation(Sham)group(6 for this group)。Sham group,only abdominal skin incision and skin closure; Bilateral femoral shaft fractures were caused by self-made device in Fracture group; Hepatic ischemia reperfusion injury was caused by Vascular liver pedicle clamping clip after 30 minutes to relax blood vessels in Hepatic Injury group; Fracture+Hepatic Injury group was fracture combining hepatic injury。Type and displacement of fracture were examed by X-ray after model completed, The expression of tumor necrosis factor-a (TNF-a)、interleukin-6(IL-6)、interleukin-10(IL-10) of hepatic tissue were detected by reverse transcription polymerase chain reaction(RT-PCR) after 1、24、48、72h of fracture management, hepatic myeloperoxidase (MPO) were detected, The contents of serum alanine aminotransferase(ALT)、lactic acid (LD) from abdominal aorta were detected. The morphological changes were observed by hematoxylin and eosin(HE)staining. PartⅡ:Thirty two SD rats were randomly divided into four groups(8 for each group):Fracture Early Surgery(FES)group、Fracture later Surgery(FLS)group、Fracture+Hepatic Injury Early Surgery(F+HIES)group、Fracture+Hepatic Injury Later Surgery,(F+HILS) group。Early surgery defined as the intramedullary nail treatment of fracture after injury 1h, later surgery defined as splint fracture after injury and the intramedullary nail treatment of fracture after injury 72h。The expression of tumor necrosis factor-a (TNF-a)、interleukin-6(IL-6)、interleukin-10(IL-10) of hepatic tissue were detected by reverse transcription polymerase chain reaction(RT-PCR) after 6h of fracture management, hepatic myeloperoxidase (MPO) were detected, The contents of serum alanine aminotransferase(ALT)、lactic acid (LD) from abdominal aorta were detected。The morphological changes were observed by hematoxylin and eosin(HE)staining。
Result:PartⅠ:X-ray shows that bilateral femoral fractures were closed fractures and significant shaft after model completed。Serum ALT、LD、MPO of three groups elevated in 1h,reached a peak in 24h,down in 48h、72h,The contents of Serum ALT、LD、MPO were significantly higher of Fracture+Hepatic Injury group than Fracture group or Hepatic Injury group (P<0.05)。The expression of tumor necrosis factor-a (TNF-a)of fracture group、hepatic injury group and fracture+hepatic injury group elevated in 1h, reached a peak in 24h,down in 48h、72h, the expression of tumor necrosis factor-a (TNF-a) of Fracture+Hepatic Injury group group was significantly higher than Fracture group or Hepatic Injury group (P<0.05); The expression of interleukin-6(IL-6) of fracture group、hepatic injury group and fracture+hepatic injury group elevated in 1h, reached a peak in 24h,down in 48h、72h, the expression of interleukin-6(IL-6) of Fracture+Hepatic Injury group was significantly higher than Fracture group or Hepatic Injury group(P<0.05); The expression of interleukin-10(IL-10) of fracture group、hepatic injury group and fracture+hepatic injury group elevated in 1h、24h、48h, reached a peak in 72h, the expression of interleukin-10(IL-10) of Fracture+Hepatic Injury group was significantly higher than Fracture group or Hepatic Injury group (P<0.05)。Rat liver biopsy in three groups shows Sinusoidal congestion、liver cell swelling,、inflammatory cell infiltration, Liver cell necrosis, inflammatory cell infiltration significantly in Fracture+Hepatic Injury group。PartⅡ:The expression of tumor necrosis factor-a (TNF-a)、interleukin-6(IL-6)、interleukin-10(IL-10)and the contents of hepatic myeloperoxidase (MPO)、serum ALT、serum LD in F+HIES group were higher than FES group or FLS group or F+HILS group (P<0.05)。The expression of tumor necrosis factor-a (TNF-a)、interleukin-6(IL-6)、interleukin-10(IL-10) and the contents of hepatic myeloperoxidase (MPO)、serum ALT、serum LD in FES group were similar with FLS group。F+HIES group of liver congestion, inflammatory cell infiltration, cell necrosis and other pathological changes significant.
Conclusion:Liver cell necrosis, inflammatory changes、pathological changes and hepatic tolerence declining of the early stage (1h)was significantly after Multiple fractures complicated with hepatic ischemia-reperfusion injury. However, hepatic tolerance enhanced in later stage (72h)。Timing of surgery effect on liver lesion after multiple fractures is small, the early fracture treatment of multiple fractures complicated with hepatic ischemia-reperfusion injury can lead to that liver lesion aggravate, treatment of damage control can increase the hepatic tolerance for the trauma and decrease liver lesion。
引文
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[32]Colletti L, Remick DG, Burtch GD, Kunkel SL, Strieter RM, Campbell DA Jr. Role of tumor necrosis factor-_ in the pathophysiologic alterations after hepatic ischemia/reperfusion injury in the rat. J Clin Invest.1990,85:1936-1943.
[33]Yoshidome H, Kato A, Edwards MJ, Lentsch AB. Interleukin-10 suppresses hepatic/ischemia reperfusion injury in mice:implications of a central role for nuclear factor kB. Hepatology.1999;30:203-208.
[34]Xu J, Yang Z, Zeng J. Role of NF-kappa B in liver ischemia reperfusion injury of rats. J Huazhong Univ Sci Technolog Med Sci 2003;23:158-160.
[35]Seekamp A,Jochurn M,Ziegler M et al. Cytokines and adhesion molecules in elective and accidental trauma-related ischemia/reperfusion. J Trauma.1998,44(5):874-882.
[36]Pallister I, Dent C, Topley N:Increased neutrophil migratory activity after major trauma:a factor in the etiology of acute respiratory distress syndrome? Crit Care Med.2002,30:1717-1721.
[37]Goris RJ:MODS/SIRS:result of an overwhelming inflammatory response? World J Surg.1996,20:418-421.
[38]Abdo EE, Cunha JE, Deluca P, et al. Protective effect of N 2 mercap top rop ionylglycine on rats and dogs liver during ischemia/reperfusion process [J]. Arq Gastroenterol,2003,40(3):177-180.
[39]McNelis J, Marini CP, Jurkiewicz A.Prolonged lactate clearance is associated with increased mortality in the surgical intensive care unit. The American Journal of Surgery.2001,182:481-485.
[40]王一镗.严重创伤救治的策略——损伤控制性手术[J].中华创伤杂志,2005(01)：33-35.
[41]Goresky, Carl A., Glen G. Bach, Andre'Simard, AndreasJ. Schwab, and Adelar Bracht. Uptake of lactate by the liver:effect of red blood cell carriage. Am J Physiol Gastrointest Liver Physiol.2000,278:775-788.
[42]. Dunham CM, Bosse MJ, Clancy TV, et al.Practice management guidelines for the optimal timing of long-bone fracture stabilization in polytrauma patients:the EAST Practice Management Guidelines Work Group[J]. J Trauma 2001,50:958-67.
[43]. Rixen D, Grass G, Sauerland S, et al.Evaluation of criteria for temporary external fixation in risk-adapted damage control orthopedic surgery of femur shaft fractures in multiple trauma patients:"Evidence-based Medicine" versus "Reality" in the Trauma Registry of the German Trauma Society[J]. J Trauma 2005, 59:1375-1395.
[44]Reynolds MA, Richardson JD, Spain DA, et al. Is the timing of fracture fixation important for the patient with multiple trauma? [J]. Ann Surg 1995;222:470—478.
[45]Ecke H, Faupel L, Quoika P. Considerations on the time of surgery of femoral fractures[J]. Unfallchirurgie 1985; 11(2):89—93.
[46]Kobbe P, Vodovotz Y, Kaczorowski DJ,et al. PATTERNS OF CYTOKINE RELEASE AND EVOLUTION OF REMOTE ORGAN DYSFUNCTION AFTER BILATERAL FEMUR FRACTURE[J]. SHOCK,2008,30(1):43-47,
[47]Sun TS, Chen XB, Liu Z. et al. Is Damage Control Orthopedics Essential for the Management of Bilateral Femoral Fractures Associated or Complicated With Shock? An Animal Study [J]. J Trauma.2009;67: 1402-1411
[48]. Liu P, Vonderfecht SL, Fisher MA, et al. Priming of phagocytes for reactive oxygen production during hepatic ischemia-reperfusion potentiates the susceptibility for endotoxin-induced liver injury[J]. Circulatory Shock.1994; 43:9.
[49].Remick DG, Colletti LM, Scales WA, et al. Cytokines and extrahepatic sequelae of ischemiareperfusion injury to the liver[J]. Ann NY Acad Sci.1994;723:271.
[50].Poeze M, Ramsay G, Buurman WA, et al. Increased hepatosplanchnic inflammation precedes the development of organ dysfunction after elective high-risk surgery[J]. Shock.2002,17:451-458.
[51]Editorial.Multiple trauma:An ongoing evolution of treatment modalities? [J]Injury, Int. J. Care Injured.2009,40:115-119
[1]Vardanian AJ, Busuttil RW, Kupiec-Weglinski JW. Molecular Mediators of Liver Ischemia and Reperfusion Injury:A Brief Review. MOL MED 2008,14 (5-6) 337-345.
[2]Moore FA, Moore EE. Evolving concepts in the pathogenesis of postinjury multiple organ failure[J]. Surg Clin N Am,1995,75 (2):275-277.
[3]Lenz A, Franklin,GA, Cheadle WG. Systemic inflammation after trauma. Injury, Int. J. Care Injured (2007) 38,1336—1345.
[4]Teoh NC,Farrell GC.Hepatic ischemia reperfusion injury:Pathogenic mechanisms and basis for hepatoprotection。Journal of Gastroenterology and Hepatology (2003) 18,891-902。
[5]Toledo-pereyra LH,Toledo AH,Walsh J et al. Molecular signaling pathways in ischemia/reperfusion. Exp Clin Transplant.2004;2(1):174-177.
[6]Singer M, De Santis V, Vitale D, Jeffcoate W. Multiorgan failure is an adaptive, endocrine-mediate, metabolic response to overwhelming systemic inflammation. Lancet 2004;364:545—8.
[7]Hubbard WJ, Bland KI, Chaudry I. THE ROLE OF THE MITOCHONDRION IN TRAUMA AND SHOCK. SHOCK,2004;22(5):395-402,
[8]Cristofori L, Tavazzi B, Gambin R, et al. Early onset of lipid peroxidation after human traumatic brain injury:a fatal limitation for the free radical scavenger pharmacological therapy? J Investig Med 2001;49:450—8.
[9]Wullaert A, van Loo G, Heyninck K, Beyaert R. Hepatic TNF signaling and NF-{kappa}B:effects on liver homeostasis and beyond. Endocr Rev.2007 Jun;28(4):365-386.
[10]Montalvo-Jave EE, Escalante-Tattersfield T, Ortega-Salgado JA,et al. FACTORS IN THE PATHOPHYSIOLOGY OF THE LIVER ISCHEMIA REPERFUSION INJURY.J Surg Res.2008 June 1; 147(1):153-159.
[11]Gao B. Cytokines, STATs and liver disease. Cell Mol Immunol 2005;2:92-100.
[12]Langdale LA, Hoagland V, Benz W,et al. Suppressor of cytokine signaling expression with increasing severity of murine hepatic ischemia-reperfusion injury. Journal of Hepatology 49 (2008) 198-206.
[13]Malhi H, Gores GJ. Cellular and Molecular Mechanisms of Liver Injury. Gastroenterology.2008,134(6): 1641-1654.
[14]Cutrn JC, Perrelli MG, Cavalieri B, Peralta C, Rosell Catafau J, Poli G. Microvascular dysfunction induced by reperfusion injury and protective effect of ischemic preconditioning. Free Radic Biol Med 2002;33:1200-8.
[15]Seekamp A,Jochum M,Ziegler M et al. Cytokines and adhesion molecules in elective and accidental trauma-related ischemia/reperfusion. J Trauma.1998,44(5):874-882.
[16]Guyton KZ, Liu Y, GorospeM, et al. Activation of mitogen-activated p rotein kinase by H2O2. Role in cell survival following oxidant injury[J]. J Biol Chem,1996,271 (8):4138-4142.
[17]Ma M,Ma ZH. Effect of tumor necrosis factor-alpha in rats with hepatic ischemia-reperfusion injury. Hepatobiliary Pancreat Dis Int 2008; 7:296-299
[18]Frink M, Pape H, van Griensven M, Krettek C, Chaudry I,Hildebrand F. Influence of sex and age on MODS and cytokines after multiple injuries. Shock 2007;27:151-156.
[19]Maier Lefering R, Lehnert M, Laurer H, Steudel W, Neugebauer E, et al. Early versus late onset of multiple organ failure is associated with differing patterns of plasma cytokine biomarker expression and outcome after severe trauma. Shock2007;28:668-674.
[20]Teoh NC,Farrell GC.Hepatic ischemia reperfusion injury:Pathogenic mechanisms and basis for hepatoprotection。Journal of Gastroenterology and Hepatology (2003) 18,891-902。
[21]Keel M, Trentz O. Pathophysiology of polytrauma. Injury, Int. J. Care Injured (2005) 36,691—709
[22]Tiberio L, Tiberio GAM, Bardella L et al. Mechanisms of interleukin-6 protection against ischemia-reperfusion injury in rat liver. Cytokine 34 (2006) 131-142
[23]Hietbrink F, Koenderman L, Rijkers GT et al. Trauma:the role of the innate immune system. World Journal of Emergency Surgery 2006,20; 1:15
[24]Donckier V,Loi P, Closset J, et al. Preconditioning of donors with interleukin-10 reduce hepatic ischemia-reperfusion injury after liver transplantation in pigs [J].Transplantation,2003,75(6):902-904.
[25]Yoshidome H, Kato A, Edwards MJ, Lentsch AB. Interleukin-10 suppresses hepatic/ischemia reperfusion injury in mice:implications of a central role for nuclear factor kB. Hepatology 1999;30:203-8.
[26]Yoshidome H, Kato A, Edwards MJ, Lentsch AB. Interleukin-10 suppresses hepatic/ischemia reperfusion injury in mice:implications of a central role for nuclear factor kB. Hepatology 1999;30:203-8.
[27]Kanoria S, Glantzounis G, Jalan R. A Model to Study Total Hepatic Ischemia-Reperfusion Injury. Transplantation Proceedings,36,2586-2589 (2004)
[28]Abdo EE, Cunha JE, Deluca P, et al. Protective effect of N 2 mercap top rop ionylglycine on rats and dogs liver during ischemia/reperfusion process [J]. Arq Gastroenterol,2003,40(3):177-180.
[29]McNelis J, Marini CP, Jurkiewicz A.Prolonged lactate clearance is associated with increased mortality in the surgical intensive care unit. The American Journal of Surgery 182 (2001) 481-485.
[30]Perdrizet GA, Giles DL, Dring R,et al. Major Hepatic Trauma:Warm Ischemic Tolerance of the Liver After Hemorrhagic Shock. Journal of Surgical Research 136,70-77 (2006)
[31]Uhlmann D, Pietsch UC, Ludwig S,et al. Assessment of hepatic ischemia-reperfusion injury by simultaneous measurement of tissue pO2, pCO2, and pH. Microvascular Research 67 (2004) 38-47。
[2]Moore FA, Sauaia A, Moore EE, Haenel JB, Burch JM and Lezotte DC. Postinjury multiple organ failure: a bimodal phenomenon. J Trauma 1996;40:501-510; discussion 510-512.
[3]Ciesla DJ ME, Johnson JL, Burch JM, Cothren CC, and Sauaia A. The role of the lung in postinjury multiple organ failure. Surgery 2005; 138:749-758.
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[5]Portella AOV, Montero EFS, Poli de Figueiredo LF. et al. Effects of N-Acetylcysteine in Hepatic Ischemia-Reperfusion Injury During Hemorrhagic Shock[J]. Transplantation Proceedings,2004,36,846-848.
[6]Mccord JM. Oxygen-derived free radicals in post ischemic tissue injury. New Engl J Med,1985,312:159.
[7]Moran A, Arikan AA, Mary-Ann A,et al. Prevention of Trauma and Hemorrhagic Shock-Mediated Liver Apoptosis by Activation of Stat3a. Int J Clin Exp Med.2008,1:213-247
[8]Bone LB, Johnson KD, Weigelt J, Scheinberg R. Early versus delayed stabilization of femoral fractures:a prospective randomized study. J Bone Joint Surg.1989;71 A:336-340.
[9]Charash WE, Fabian TC, Croce MA. Delayed surgical fixation of femur fractures is a risk factor for pulmonary failure independent of thoracic trauma. J Trauma.1994;37:667-672.
[10]Taeger G, Ruchholtz S, Zettl R, Waydhas C, Nast-Kolb D. Prima'rer Fixateur externe mit konsekutivem Verfahrenswechsel beim Polytrauma. Unfallchirurg.2002; 105:315-321.
[11]Scalea TM, Boswell SA, Scott JD, et al. External fixation as a bridge to intramedullary nailing for patients with multiple injuries and with femur fractures:damage control orthopedics. J Trauma.2000;48:613-623.
[12]Faist E, Baue AE, Dittmer H, et al. Multiple organ failure in polytrauma patients[J]. J Trauma.1983,23:775-787.
[13]Giannoudis PV, Smith RM, Bellamy MC, et al. Stimulation of the inflammatory system by reamed and unreamed nailing of femoral fractures-an analysis of the second hit. J Bone Joint Surg Br.1999; 81:356-361. 。
[14]Pape HC, van Griensven M, Sott AH, et al. Impact of intramedullary instrumentation versus damage control for femoral fractures on immunoinflammatory parameters:prospective randomized analysis by the EPOFF study group. J Trauma.2003;55:7-13.
[15]Portella AOV, Montero EFS, Figueiredo LFPD,et al.Effects of N-Acetylcysteine in Hepatic Ischemia-Reperfusion Injury During Hemorrhagic Shock[J]. Transplantation Proceedings,2004,36:846-848.
[16]Thomas M. Scalea, MD, FACS. Optimal Timing of Fracture Fixation:Have We Learned Anything In the Past 20 Years? J Trauma.2008;65:253-260.
[17]YANG J, GAO JM, HU P.et al. Application of damage control orthopedics in 41 patients with severe multiple injuries. Chinese Journal of Traumatology 2008; 11(3):157-160
[18]Bose D, Tejwani NC. Evolving trends in the care of polytrauma Patients. Injury, Int. J. Care Injured.2006,37:20—28
[19]Ma m,Ma ZH. Effect of tumor necrosis factor-alpha in rats with hepatic ischemia-reperfusion injury[J]. Hepatobiliary Pancreat Dis Int 2008; 7:296-299
[20]Copeland CE, Mitchell KA, Brumback RJ, et al. Mortality in patients with bilateral femoral fractures[J]. J Orthop Trauma.1998,12:315-319.
[21]Kanoria S, Glantzounis G, Jalan R, et al.A Model to Study Total Hepatic Ischemia-Reperfusion Injury [J]. Transplantation Proceedings.2004,36:2586-2589.
[22]Yamakawa Y, Takano M, Patel M, et al. Interaction of Platelet Activating Factor, Reactive Oxygen Species Generated by Xanthine Oxidase, and Leukocytes in the Generation of Hepatic Injury After Shock/Resuscitation. ANNALS OF SURGERY,2000,231:387-398
[23]Moore FA, Moore EE. Evolving concepts in the pathogenesis of postinjury multiple organ failure[J]. Surg Clin N Am.1995,75 (2):275-277.
[24]Guan J, Jin DD, Jin LJ, Lu Q:Apoptosis in organs of rats in early stage after polytrauma combined with shock. J Trauma.2002,52:104-111.
[25]Matsutani T, Kang SC, Miyashita M, Sasajima K, Choudhry MA, Bland KI, Chaudry IH:Liver cytokine production and ICAM-1 expression following bone fracture, tissue trauma, and hemorrhage in middle-aged mice. Am J Physiol Gastrointest Liver Physiol.2007,292:268-274.
[26]Kanoria S, Glantzounis G, Jalan R.etal. A Model to Study Total Hepatic Ischemia-Reperfusion Injury. Transplantation Proceedings.2004,36,2586-2589.
[27]Helewski KJ, Kowalczyk-Ziomek GI, Konecki J.Neutrophils' contribution to ischaemia and reperfusion injury in liver. Wiad Lek.2007,60:47-52.
[28]HendersonHenderson JM. Liver transplantation and rejection:an overview. Hepatogastroenterology. 1999,46:1482-1484.
[29]Uhlmann D, Gabel G, Ludwig S, Armann B, Hess J, Pietsch UC, et al. Effects of ET(A) receptor antagonism on proinflammatory gene expression and microcirculation following hepatic ischemia/reperfusion. Microcirculation.2005,12:405-419.
30] Hatano E. Tumor necrosis factor signaling in hepatocyte apoptosis. J Gastroenterol Hepatol.2007,22:43-44.
[31]Suzuki S, Toledo-Pereyra LH. Interleukin 1 and tumor necrosis factor production as the initial stimulants of liver ischemia and reperfusion injury. J Surg Res.1994,57:253-258.
[32]Colletti L, Remick DG, Burtch GD, Kunkel SL, Strieter RM, Campbell DA Jr. Role of tumor necrosis factor-_ in the pathophysiologic alterations after hepatic ischemia/reperfusion injury in the rat. J Clin Invest.1990,85:1936-1943.
[33]Yoshidome H, Kato A, Edwards MJ, Lentsch AB. Interleukin-10 suppresses hepatic/ischemia reperfusion injury in mice:implications of a central role for nuclear factor kB. Hepatology.1999;30:203-208.
[34]Xu J, Yang Z, Zeng J. Role of NF-kappa B in liver ischemia reperfusion injury of rats. J Huazhong Univ Sci Technolog Med Sci 2003;23:158-160.
[35]Seekamp A,Jochurn M,Ziegler M et al. Cytokines and adhesion molecules in elective and accidental trauma-related ischemia/reperfusion. J Trauma.1998,44(5):874-882.
[36]Pallister I, Dent C, Topley N:Increased neutrophil migratory activity after major trauma:a factor in the etiology of acute respiratory distress syndrome? Crit Care Med.2002,30:1717-1721.
[37]Goris RJ:MODS/SIRS:result of an overwhelming inflammatory response? World J Surg.1996,20:418-421.
[38]Abdo EE, Cunha JE, Deluca P, et al. Protective effect of N 2 mercap top rop ionylglycine on rats and dogs liver during ischemia/reperfusion process [J]. Arq Gastroenterol,2003,40(3):177-180.
[39]McNelis J, Marini CP, Jurkiewicz A.Prolonged lactate clearance is associated with increased mortality in the surgical intensive care unit. The American Journal of Surgery.2001,182:481-485.
[40]王一镗.严重创伤救治的策略——损伤控制性手术[J].中华创伤杂志,2005(01)：33-35.
[41]Goresky, Carl A., Glen G. Bach, Andre'Simard, AndreasJ. Schwab, and Adelar Bracht. Uptake of lactate by the liver:effect of red blood cell carriage. Am J Physiol Gastrointest Liver Physiol.2000,278:775-788.
[42]. Dunham CM, Bosse MJ, Clancy TV, et al.Practice management guidelines for the optimal timing of long-bone fracture stabilization in polytrauma patients:the EAST Practice Management Guidelines Work Group[J]. J Trauma 2001,50:958-67.
[43]. Rixen D, Grass G, Sauerland S, et al.Evaluation of criteria for temporary external fixation in risk-adapted damage control orthopedic surgery of femur shaft fractures in multiple trauma patients:"Evidence-based Medicine" versus "Reality" in the Trauma Registry of the German Trauma Society[J]. J Trauma 2005, 59:1375-1395.
[44]Reynolds MA, Richardson JD, Spain DA, et al. Is the timing of fracture fixation important for the patient with multiple trauma? [J]. Ann Surg 1995;222:470—478.
[45]Ecke H, Faupel L, Quoika P. Considerations on the time of surgery of femoral fractures[J]. Unfallchirurgie 1985; 11(2):89—93.
[46]Kobbe P, Vodovotz Y, Kaczorowski DJ,et al. PATTERNS OF CYTOKINE RELEASE AND EVOLUTION OF REMOTE ORGAN DYSFUNCTION AFTER BILATERAL FEMUR FRACTURE[J]. SHOCK,2008,30(1):43-47,
[47]Sun TS, Chen XB, Liu Z. et al. Is Damage Control Orthopedics Essential for the Management of Bilateral Femoral Fractures Associated or Complicated With Shock? An Animal Study [J]. J Trauma.2009;67: 1402-1411
[48]. Liu P, Vonderfecht SL, Fisher MA, et al. Priming of phagocytes for reactive oxygen production during hepatic ischemia-reperfusion potentiates the susceptibility for endotoxin-induced liver injury[J]. Circulatory Shock.1994; 43:9.
[49].Remick DG, Colletti LM, Scales WA, et al. Cytokines and extrahepatic sequelae of ischemiareperfusion injury to the liver[J]. Ann NY Acad Sci.1994;723:271.
[50].Poeze M, Ramsay G, Buurman WA, et al. Increased hepatosplanchnic inflammation precedes the development of organ dysfunction after elective high-risk surgery[J]. Shock.2002,17:451-458.
[51]Editorial.Multiple trauma:An ongoing evolution of treatment modalities? [J]Injury, Int. J. Care Injured.2009,40:115-119
[1]Vardanian AJ, Busuttil RW, Kupiec-Weglinski JW. Molecular Mediators of Liver Ischemia and Reperfusion Injury:A Brief Review. MOL MED 2008,14 (5-6) 337-345.
[2]Moore FA, Moore EE. Evolving concepts in the pathogenesis of postinjury multiple organ failure[J]. Surg Clin N Am,1995,75 (2):275-277.
[3]Lenz A, Franklin,GA, Cheadle WG. Systemic inflammation after trauma. Injury, Int. J. Care Injured (2007) 38,1336—1345.
[4]Teoh NC,Farrell GC.Hepatic ischemia reperfusion injury:Pathogenic mechanisms and basis for hepatoprotection。Journal of Gastroenterology and Hepatology (2003) 18,891-902。
[5]Toledo-pereyra LH,Toledo AH,Walsh J et al. Molecular signaling pathways in ischemia/reperfusion. Exp Clin Transplant.2004;2(1):174-177.
[6]Singer M, De Santis V, Vitale D, Jeffcoate W. Multiorgan failure is an adaptive, endocrine-mediate, metabolic response to overwhelming systemic inflammation. Lancet 2004;364:545—8.
[7]Hubbard WJ, Bland KI, Chaudry I. THE ROLE OF THE MITOCHONDRION IN TRAUMA AND SHOCK. SHOCK,2004;22(5):395-402,
[8]Cristofori L, Tavazzi B, Gambin R, et al. Early onset of lipid peroxidation after human traumatic brain injury:a fatal limitation for the free radical scavenger pharmacological therapy? J Investig Med 2001;49:450—8.
[9]Wullaert A, van Loo G, Heyninck K, Beyaert R. Hepatic TNF signaling and NF-{kappa}B:effects on liver homeostasis and beyond. Endocr Rev.2007 Jun;28(4):365-386.
[10]Montalvo-Jave EE, Escalante-Tattersfield T, Ortega-Salgado JA,et al. FACTORS IN THE PATHOPHYSIOLOGY OF THE LIVER ISCHEMIA REPERFUSION INJURY.J Surg Res.2008 June 1; 147(1):153-159.
[11]Gao B. Cytokines, STATs and liver disease. Cell Mol Immunol 2005;2:92-100.
[12]Langdale LA, Hoagland V, Benz W,et al. Suppressor of cytokine signaling expression with increasing severity of murine hepatic ischemia-reperfusion injury. Journal of Hepatology 49 (2008) 198-206.
[13]Malhi H, Gores GJ. Cellular and Molecular Mechanisms of Liver Injury. Gastroenterology.2008,134(6): 1641-1654.
[14]Cutrn JC, Perrelli MG, Cavalieri B, Peralta C, Rosell Catafau J, Poli G. Microvascular dysfunction induced by reperfusion injury and protective effect of ischemic preconditioning. Free Radic Biol Med 2002;33:1200-8.
[15]Seekamp A,Jochum M,Ziegler M et al. Cytokines and adhesion molecules in elective and accidental trauma-related ischemia/reperfusion. J Trauma.1998,44(5):874-882.
[16]Guyton KZ, Liu Y, GorospeM, et al. Activation of mitogen-activated p rotein kinase by H2O2. Role in cell survival following oxidant injury[J]. J Biol Chem,1996,271 (8):4138-4142.
[17]Ma M,Ma ZH. Effect of tumor necrosis factor-alpha in rats with hepatic ischemia-reperfusion injury. Hepatobiliary Pancreat Dis Int 2008; 7:296-299
[18]Frink M, Pape H, van Griensven M, Krettek C, Chaudry I,Hildebrand F. Influence of sex and age on MODS and cytokines after multiple injuries. Shock 2007;27:151-156.
[19]Maier Lefering R, Lehnert M, Laurer H, Steudel W, Neugebauer E, et al. Early versus late onset of multiple organ failure is associated with differing patterns of plasma cytokine biomarker expression and outcome after severe trauma. Shock2007;28:668-674.
[20]Teoh NC,Farrell GC.Hepatic ischemia reperfusion injury:Pathogenic mechanisms and basis for hepatoprotection。Journal of Gastroenterology and Hepatology (2003) 18,891-902。
[21]Keel M, Trentz O. Pathophysiology of polytrauma. Injury, Int. J. Care Injured (2005) 36,691—709
[22]Tiberio L, Tiberio GAM, Bardella L et al. Mechanisms of interleukin-6 protection against ischemia-reperfusion injury in rat liver. Cytokine 34 (2006) 131-142
[23]Hietbrink F, Koenderman L, Rijkers GT et al. Trauma:the role of the innate immune system. World Journal of Emergency Surgery 2006,20; 1:15
[24]Donckier V,Loi P, Closset J, et al. Preconditioning of donors with interleukin-10 reduce hepatic ischemia-reperfusion injury after liver transplantation in pigs [J].Transplantation,2003,75(6):902-904.
[25]Yoshidome H, Kato A, Edwards MJ, Lentsch AB. Interleukin-10 suppresses hepatic/ischemia reperfusion injury in mice:implications of a central role for nuclear factor kB. Hepatology 1999;30:203-8.
[26]Yoshidome H, Kato A, Edwards MJ, Lentsch AB. Interleukin-10 suppresses hepatic/ischemia reperfusion injury in mice:implications of a central role for nuclear factor kB. Hepatology 1999;30:203-8.
[27]Kanoria S, Glantzounis G, Jalan R. A Model to Study Total Hepatic Ischemia-Reperfusion Injury. Transplantation Proceedings,36,2586-2589 (2004)
[28]Abdo EE, Cunha JE, Deluca P, et al. Protective effect of N 2 mercap top rop ionylglycine on rats and dogs liver during ischemia/reperfusion process [J]. Arq Gastroenterol,2003,40(3):177-180.
[29]McNelis J, Marini CP, Jurkiewicz A.Prolonged lactate clearance is associated with increased mortality in the surgical intensive care unit. The American Journal of Surgery 182 (2001) 481-485.
[30]Perdrizet GA, Giles DL, Dring R,et al. Major Hepatic Trauma:Warm Ischemic Tolerance of the Liver After Hemorrhagic Shock. Journal of Surgical Research 136,70-77 (2006)
[31]Uhlmann D, Pietsch UC, Ludwig S,et al. Assessment of hepatic ischemia-reperfusion injury by simultaneous measurement of tissue pO2, pCO2, and pH. Microvascular Research 67 (2004) 38-47。