维拉帕米对大鼠创伤失血性休克复合内毒素血症模型的保护作用

目的　研究钙通道阻滞剂维拉帕米对创伤失血性休克复合内毒素血症模型大鼠的保护作用。方法　制作大鼠创伤失血性休克复合内毒素血症动物模型 ,腹腔内给予维拉帕米干预治疗 ,检测血清中TNF -α、IL - 1β、IL - 10含量的变化及大鼠肺组织的病理改变。结果　维拉帕米干预治疗组大鼠血清中TNF -α、IL - 1β的水平较致伤组明显降低 (P <0 .0 1) ,血清中IL - 10的含量较致伤组明显升高 (P <0 .0 1) ,大鼠肺组织炎症病理改变较致伤组明显减轻。结论　维拉帕米干预治疗对大鼠创伤失血性休克复合内毒素模型有明显保护作用。     

大鼠创伤失血性休克复合内毒素打击模型中p38丝裂原活化蛋白激酶磷酸化水平的改变

目的　探讨创伤失血性休克复合内毒素打击模型中大鼠腹腔巨噬细胞 (M)内p38丝裂原活化蛋白激酶(p38MAPK)磷酸化水平的改变。方法　制作大鼠创伤失血性休克复合内毒素打击动物模型 ,检测伤后 90min、4h血清中TNF-α、IL - 1β含量的改变及大鼠腹腔M内p38MAPK磷酸化水平的变化 ,并观察致伤组大鼠肺及小肠组织的病理改变。 结果　大鼠在创伤失血性休克复合内毒素打击后血清TNF -α、IL - 1β的含量较对照组明显升高 (P <0 .0 1) ,腹腔M内p38MAPK磷酸化水平较对照组明显升高 (P <0 .0 1) ,致伤组大鼠肺及小肠组织炎症病理改变显著。结论　p38MAPK的激活状态可能在大鼠创伤失血性休克复合内毒素打击模型的炎症反应中占有重要地位。     

地塞米松对大鼠创伤失血性休克模型的保护作用

目的探讨早期大剂量地塞米松对大鼠创伤失血性休克的保护作用.方法制作创伤失血性休克大鼠动物模型,随机分为正常对照组(A组)、创伤失血性休克组(B组)、创伤失血性休克地塞米松处理组(C组).分别于模型完成的1、2、3、6、12 h时间点测血浆肿瘤坏死因子-α(TNF-α)、白细胞介素(IL)-1β、IL-10水平,取肺、脾做光镜检查.结果大鼠遭受创伤失血性休克打击后,血浆TNF-α水平持续增高,6 h达高峰;IL-1β、IL-10持续增高;光镜下肺损伤,脾小体萎缩、坏死,败血脾.地塞米松能显著降低血浆TNF-α、IL-1β、IL-10的表达水平,减轻脾、肺组织损伤,脾小体持续增生.结论早期大剂量地塞米松抑制过度炎症反应的同时,抑制IL-10的高水平表达,显示了较好的免疫调理作用.     

淋巴液对内毒素休克大鼠的干预作用及其机制

目的　观察外源性正常淋巴液对脂多糖 (LPS)所致大鼠内毒素休克的干预作用 ,初步探讨其作用机制。方法　Wistar雄性大鼠 4 0只 ,随机分为内毒素组、淋巴液组、血浆组、正常组。前 3组复制内毒素休克模型 (LPS ,5mg/kg·bw ,iv) ,正常组以等量生理盐水代替LPS。 15min后 ,淋巴液组输入仅占全血量 1/ 15的无细胞淋巴液。血浆组以血浆代替淋巴液 ,内毒素组和正常组以生理盐水代替淋巴液。给予LPS后 4h,取血浆及心、肝、肾、肺组织匀浆 ,对比观察血浆及组织中肿瘤坏死因子 -α(TNF -α)、一氧化氮 (NO)、一氧化氮合酶 (NOS)、诱导型一氧化氮合酶 (iNOS)、超氧化物歧化酶 (SOD)及丙二醛 (MDA)含量的变化。结果　淋巴液干预后 ,淋巴液组血浆TNF -α水平为 18.81± 3.70fmol/mL、NO含量为 4 6 .0 2± 9.2 9μmol/L、NOS活性为 2 5 .16± 4 .2 0U/mL、SOD活性为 10 2 .15± 17.88NU/mL、MDA水平 8.19± 1.6 4nmol/mL ,与其余 3组相比 ,各项指标差异均有统计学意义 (P <0 .0 5～ 0 .0 1)。结论　外源性正常淋巴液对内毒素休克具有干预作用 ,其机制可能与减少细胞因子及自由基损伤有关。     

p38MAPK抑制剂对钛颗粒刺激巨噬细胞分泌炎症因子的影响

目的:探讨p38MAPK抑制剂(SB203580)对外培养的RAW246.7细胞分泌炎症因子[肿瘤坏死因子-α(TNF-α)、白介素-6(IL-6)]的影响。方法:以体外正常培养RAW246.7细胞为A组,以0.1 mg/m L钛颗粒(Ti Ps)刺激RAW246.7细胞为B组,以10μmol/L SB203580干预的B组细胞为C组。Western blot检测p-p38MAPK蛋白表达,ELISA检测细胞分泌TNF-α,IL-6水平。结果:与A组比较,B组p-p38MAPK蛋白含量培养液上清中TNF-α、IL-6含量都明显升高(P<0.05);与B组比较,C组p-p38MAPK蛋白明显抑制(P<0.05),培养液上清中TNF-α、IL-6含量都明显下降(P<0.05);与A组比较,C组p-p38MAPK蛋白明显抑制(P<0.05),培养液上清中TNF-α、IL-6含量亦有所减少,但两组之间的差异没有统计学意义(P>0.05)。结论:Ti Ps能通过刺激RAW246.7细胞,激活p38MAPK通路,上调TNF-α、IL-6等炎症因子的表达。p38MAPK信号通路可作为抑制炎性骨溶解的新靶点,对临床上防治人工关节置换术后无菌性松动具有重要意义。     

眼镜蛇毒因子抑制补体激活对创伤失血性休克大鼠血浆内毒素含量的影响

目的观察眼镜蛇毒因子（CVF）抑制补体激活对创伤失血性休克大鼠血浆内毒素含量的影响。方法80只雄性SD大鼠随机分成对照组和CVF组。建立刨伤失血性休克模型，于休克前及复苏后1、6和24h取血．检测血浆内毒素（LPS）、血清肿瘤坏死因子-α（TNF-α）含量及血清二胺氧化酶（DAO）和总补体活性（CH50）。结果对照组大鼠复苏后1h血CH50水平迅速下降，血LPS、TNF—α水平均明显升高，随后均快速恢复至休克前水平;DAO活性在复苏后1h和6h明显升高，然后快速下降。CVF组大鼠除CH50水平始终〈5％，其余各指标复苏后1h仅略升高，复苏后各时间点均较对照组相应时间点明显降低（P〈0．05或P〈0．01）。结论在创伤失血性休克中使用补体抑制剂CVF可明显减轻补体激活导致的肠道损伤及肠屏障破坏，减少LPS移位的发生，明显降低血浆LPS含量。     

创伤失血性休克大鼠T淋巴细胞功能变化及地塞米松对其影响

目的探讨创伤失血性休克大鼠T淋巴细胞的功能变化及地塞米松对其影响。方法制作创伤失血性休克大鼠动物模型,大鼠随机分为正常对照组、创伤失血性休克组、创伤失血性休克地塞米松处理组。分别于模型完成的1、2、3、6、12h时间点测血浆肿瘤坏死因子-α(TNF-α)水平,将各组各时间点大鼠活取肺、脾做病理学检查,取2、6h时间点创伤失血性休克组脾做电镜检查。并取各组各时间点脾做免疫组化白细胞介素-2(IL-2)、白细胞介素-4(IL-4)标记。结果大鼠遭受创伤失血性休克打击后,血浆TNF-α水平持续增高,6h达高峰。光镜下肺脏组织损伤,脾小体早期增生,后期出现萎缩。电镜显示脾小体增生期脾淋巴细胞增殖活化,脾小体萎缩期脾淋巴细胞坏死。免疫组化显示脾小体增生期以IL-2表达为主,萎缩期以IL-4表达为主。地塞米松能显著降低血浆TNF-α表达水平,减轻脾、肺组织损伤,脾小体持续增生,免疫组化标记结果变化不大。结论创伤失血性休克大鼠早期T淋巴细胞激活,随后出现了向TH2的漂移,最后淋巴细胞功能衰竭。通过早期应用地塞米松抑制了过度的炎症反应,保存了淋巴细胞的功能。     

内毒素血症细胞因子一氧化氮在重度失血性休克发展中的作用

目的　探讨内毒素血症、细胞因子、ＮＯ在重度失血性休克发展过程中的作用和机制。方法　选用大白兔２６只,分为失血性休克组（１４ 只）,对照组（１２ 只）,休克组观察休克前后血浆内毒素、ＴＮＦα、ＩＬ－ ６、ＩＬ－８、ＮＯ的动态变化,对照组观察手术前后上述指标的变化,两组动物均观察２４ 小时、４８ 小时存活率。结果　大白兔发生失血性休克后血浆内毒素、ＴＮＦα、ＩＬ－６、ＩＬ－８ 、ＮＯ的水平与休克前及对照组比较有明显升高,死亡动物中血浆上述物质水平显著高于存活动物。结论　内毒素血症、细胞因子、ＮＯ等发挥重要的协同作用,促使失血性休克向不可逆方向进展。     

眼镜蛇毒因子对创伤失血性休克大鼠肠道的作用

目的观察眼镜蛇毒因子（CVF）抑制补体激活对创伤失血性休克大鼠肠道的影响。方法雄性SD大鼠建立创伤失血性休克模型,随机分成对照组和CVF组,根据观察时间点的不同各组再分为休克前、复苏后1、6、24h时相组。结果对照组大鼠复苏后1h血总补体活性（CH50）水平迅速下降,血内毒素（LPS）浓度、肠黏膜损伤评分均明显升高,随后2个时间点快速恢复至休克前水平;二胺氧化酶（DAO）活性在随后1h和6h时相明显升高,然后快速下降。CVF组大鼠除CH50水平始终〈5％,其余各指标复苏后1h仅略升高,其复苏后各时相组均较对照组相应时相组明显降低。结论在创伤失血性休克中使用补体抑制剂可明显减轻补体激活导致的肠道损伤及肠屏障破坏,减少内毒素移位的发生,明显降低血浆内毒素含量。     

乌司他丁对失血性休克复合内毒素模型兔肺组织中核因子-κB的影响

目的 探讨失血性休克复合内毒素打击兔急性肺损伤(ALI)中核因子-KB(NF-κB)的活化和肿瘤坏死因子-α(TNF-α)的释放及乌司他丁的抑制作用.方法 失血性休克复合内毒素打击法复制AU兔模型:90只兔随机分为对照组(A组)、创伤组(B组)和乌司他丁组(C组).各时相点检测动脉血氧分压(PaO2)、肺干质量/湿质量比值(D/W)、血清TNF-α浓度、肺组织内NF-κB的变化情况,并进行肺大体外观及组织病理学光镜检查.结果 与A组比较,B组PaO2进行性下降,C组Pao2于4 h达到最低值后逐渐上升;B组血清TNF-α含量及肺组织NF-κB p65的表达升高,并均于4 h达到最高峰(P<0.01),C组24 h、48 h时TNF-α含量及NF-κBp65的表达较B组明显降低(P<0.05).C组动物肺损伤程度明显减轻.结论 乌司他丁可通过抑制NF-κB活化,减少TNF-α等炎性介质的释放从而减轻肺损伤.     

胸腺五肽对重度创伤失血性休克大鼠SIgA的影响

目的 探讨早期加用胸腺五肽(TP-5)对重度创伤失血性休克大鼠SIgA的影响.方法 72只健康雄性SD大鼠随机分为常规复苏组和TP-5复苏组,每组36例.常规复苏组选用乳酸林格液复苏;TP-5复苏组在常规复苏的基础上早期加用TP-5.在休克前(t0)、休克复苏前(t1)及休克复苏或复苏给药后12 h(t2)、24 h(t3)、48 h(t4)、72 h(t5)各时间点采集肠道黏液,应用ELISA试剂盒测定SIgA含量,并在光学显微镜下进行小肠上皮损伤指数评分.结果 与休克前比较,复苏前后两组SIgA含量均明显降低(P<0.01),随复苏时间的延长,SIgA含量逐渐升高,两组复苏后12 h、24 h、48 h、72 h比较差异有统计学意义(P<0.05).两组休克复苏前及复苏后12 h、24 h、48 h小肠上皮损伤指数均明显升高(P<0.05,P<0.01),随复苏时间的延长,小肠上皮损伤指数逐渐回降,TP-5组复苏后24 h、48 h明显优于常规复苏组(P<0.05).结论 重度创伤失血性休克大鼠复苏早期联合应用TP-5较常规复苏治疗可显著提高SIgA的分泌量,加快小肠黏膜形态、结构完整性的恢复,保护肠道黏膜屏障,有益于提高机体免疫能力.     

不同液体复苏方式治疗创伤失血性休克的疗效分析

目的探讨不同液体复苏方式对创伤失血性休克早期的治疗效果。方法回顾性分析2002年7月至2005年7月广东省人民医院收治的72例患者,随机采用常规液体复苏(常规组)和限制性液体复苏(限制组)两种不同复苏方式,对两组患者的红细胞压积、血清乳酸、血气剩余碱值(BE)、输入液体量和失血量进行统计学分析,比较限制性液体复苏与常规液体复苏对失血性休克患者的临床疗效。结果采用两种不同复苏方式治疗后,两组患者的红细胞压积、血清乳酸、BE等变化幅度的差异具有统计学意义(P<0.05);常规组在进行手术前输液量为(27484±649)ml,限制组在进行手术前输液量为(1863±672)ml,两组比较差异有统计学意义(t=2.93,P<0.05);常规组病死率为18.9%,限制组病死率为11.4%,差异有统计学意义(χ2=4.23,P<0.05)。结论在出血未控制的情况下,限制性液体复苏可维持重要脏器的血流灌注,为进一步治疗赢得时间,改善预后,降低病死率。     

血小板活化因子拮抗剂对急性出血坏死型胰腺炎大鼠内毒素血症的防治作用

目的：观察血小板活化因子（ＰＡＦ）拮抗剂对急性出血坏死型胰腺炎（ＡＨＮＰ）大鼠内毒素血症的防治作用。方法：１４０只ＳＤ大鼠随机分为３组：急性胰腺炎组（ＡＰ组）：采用去氧胆酸钠逆行胰管内注射法复制；治疗组（ＢＮ组）：制备模型后经腹腔注射ＰＡＦ特异性受体拮抗剂ＢＮ５２０２１（５ｍｇ／ｋｇ）；假手术组（ＳＯ组）：开腹后仅轻轻翻动胰腺即关腹。结果：ＢＮ组与ＡＰ组比较，１小时后血清淀粉酶值明显下降〔（１４９７０±２５００）Ｕ／Ｌ，（１６１７０±２３８０）Ｕ／Ｌ，Ｐ＜０．０５〕，６小时和１２小时后更为明显（Ｐ均＜０．０１）；血中ＰＡＦ含量１小时后明显降低〔（２．２０±０．２５）μｇ／Ｌ与（１．１０±０．２１）μｇ／Ｌ，Ｐ＜０．０５〕，３小时后更为明显（Ｐ＜０．０１）。血浆内毒素含量ＢＮ组比ＡＰ组明显下降（Ｐ＜０．０１）。ＢＮ组术后大鼠平均存活时间为（４５．０±２５．１）小时，存活率为４０％；ＡＰ组术后大鼠在２４小时内全部死亡，平均存活时间为（１１．５±４．８）小时，存活率为０（Ｐ均＜０．０１）。结论：ＰＡＦ参与了ＡＨＮＰ的发病过程；应用ＰＡＦ受体拮抗剂对实验性ＡＨＮＰ有良好的防治作用。     

胸腹联合伤合并创伤失血性休克的液体复苏治疗

目的探讨延迟与即刻液体复苏对胸腹联合伤并创伤性休克患者的早期救治效果。方法回顾性分析2004年11月至2006年12月来院救治的98例胸腹联合伤并创伤性休克患者资料,所有病例均符合第五版《外科学》休克诊断标准。延迟复苏组（n=51）,在到达手术室彻底止血前,只给予少量的平衡液维持机体基本需求;即刻复苏组（n=47）,入院后快速给予大量等张晶体液和（或）胶体液。用成组t检验、方差分析或χ^2检验分析两种液体复苏方式对血红蛋白含量、血小板计数、红细胞比容、血乳酸含量、碱缺失水平、术前复苏时间及病死率的影响。结果延迟复苏组与即刻复苏组输液量差异具有统计学意义[（1586±346）vs（3520±575）ml,P〈0．01],但两组患者在手术前收缩压却差异无统计学意义[（78±29）mmHgvs（81±24）mmHg,P〉0．05]。术前血红蛋白[（106．21±20．91）g/Lvs（89．10±32．42）g／L]、凝血酶原时间[（11．19±2．03）svs（17．37±2．50）s]、血小板计数[（179．44±52．19）×10^9/Lvs（105．55±50．67）×10^9/L]、红细胞比容[（28．40±2．31）％vs（20．84±2．58）％]、血乳酸[复苏30min：（1．70±0．37）mmol／Lvs（2．44±0．41）mmol／L;复苏60min：（3．16±0．42）mmol／Lvs（5．73±0．68）mmol／L]和碱缺失[复苏30min：（-4．46±1．15）mmol／LVs（-5．78±1．15）mmol／L;复苏60min：（-5．46±1．29）mmol／Lvs（-9．60±2．71）mmol／L],两组间差异具有统计学意义（P〈0．05）。即刻复苏组术前复苏时间（73±29）min、病死率（18．9％）,延迟复苏组术前复苏时间（58±26）min、病死率（11．3％）,组间比较差异有统计学意义（P〈0．05）。结论延迟液体复苏能显著改善胸腹联合伤并创伤失血性休克患者凝血功能、组织和器官的灌注及乳酸酸中毒程度,降低患者的病死率,缩短术前复苏时间,效果优于即刻液体复苏。     

限制性液体复苏对肝脏缺血-再灌注损伤的影响

Objective To investigate the effects of limited resuscitation on hepatic ischernia-reperfusion in-jury in rots with hemorrhagic shock. Method Uncontrolled hemorrhagic shock was induced in 54 rats by transect-ing the middle branch of the splenic artery to produce standardized massive splenic injury. Resuscitation started when the mean arterial pressure (MAP) reached 40 mmHg. The rats were randomly divided (n = 9per group) in-to sham-operated group (SS), or one of five treatment groups in which infusion of Ringer' s solution was continually administrated to maintain MAP at 40 (RS40), 50 (RS50), 60 (RS60), 80 (RS80) or 100 mmHg (RS100) for 45 minutes (T45 point). After the bleeding was controlled, resuscitation was continued with Ringer's solution and whole blood (2:1) to increase the MAP to 100 mmHg for 120 minutes (T165 point), which was followed by obser-vation for 240 minutes (T405 point). All animals were observed for 240 minutes or until death. Blood specimens were collected at TO, T45, T165 and T405 for determination of blood lactate levels. At the end of the experiment,a small amount of hepatic tissue was collected to measure tissue blood perfusion, total antioxidative capacity (TAOC), Na+K+ ATPase activity and malondialdehyde (MDA) levels. Results At T405, the blood lactate lev-els in the RS80 and RS100 groups [(3.60±0.68) and (3.84 ± 1.09) mmol/L, respectively] were significantly higher than those in the SS, RS40, RS50 and RS60 groups [(2.00±0.66),(2.74±1.45),(2.43 +0.94) and (2.07±0.95) mmol/L, respectively;all:P < 0.05]. The MDA levels were significantly higher in the RS80 and RS100[(7.32±0.31) and (7.71±0.23) nmol/mg,respectively] than those in the SS, RS40, RS50 and RS60 groups[(4.95±0.80),(6.14±0.94),(6.42±0.48) and (6.84±0.36) nmol/mg, respeetively;all: P <0.05]. The Na+ K+ ATPase and TAOC levels were significantly lower in all of the RS groups than those in the SS group (all: P < 0.05), and those in the RS80 and RS100 groups was significantly lower than those in the RS40,RS50 and RS60 groups (all: P <0.05). Blood perfusion in the RS80 and RS100 groups was significantly lower than that in the other groups (all: P < 0.05). Conclusions If hemorrhage is uncontrolled, limited resuscitation appears to balance the needs for organ perfusion, improve the microcircttlation and decrease lactate levels. Fur-thermore, limited resuscitation could decrease ischemia-reperfusion injury in liver tissue.     

限制性液体复苏对肝脏缺血-再灌注损伤的影响

Objective To investigate the effects of limited resuscitation on hepatic ischernia-reperfusion in-jury in rots with hemorrhagic shock. Method Uncontrolled hemorrhagic shock was induced in 54 rats by transect-ing the middle branch of the splenic artery to produce standardized massive splenic injury. Resuscitation started when the mean arterial pressure (MAP) reached 40 mmHg. The rats were randomly divided (n = 9per group) in-to sham-operated group (SS), or one of five treatment groups in which infusion of Ringer' s solution was continually administrated to maintain MAP at 40 (RS40), 50 (RS50), 60 (RS60), 80 (RS80) or 100 mmHg (RS100) for 45 minutes (T45 point). After the bleeding was controlled, resuscitation was continued with Ringer's solution and whole blood (2:1) to increase the MAP to 100 mmHg for 120 minutes (T165 point), which was followed by obser-vation for 240 minutes (T405 point). All animals were observed for 240 minutes or until death. Blood specimens were collected at TO, T45, T165 and T405 for determination of blood lactate levels. At the end of the experiment,a small amount of hepatic tissue was collected to measure tissue blood perfusion, total antioxidative capacity (TAOC), Na+K+ ATPase activity and malondialdehyde (MDA) levels. Results At T405, the blood lactate lev-els in the RS80 and RS100 groups [(3.60±0.68) and (3.84 ± 1.09) mmol/L, respectively] were significantly higher than those in the SS, RS40, RS50 and RS60 groups [(2.00±0.66),(2.74±1.45),(2.43 +0.94) and (2.07±0.95) mmol/L, respectively;all:P < 0.05]. The MDA levels were significantly higher in the RS80 and RS100[(7.32±0.31) and (7.71±0.23) nmol/mg,respectively] than those in the SS, RS40, RS50 and RS60 groups[(4.95±0.80),(6.14±0.94),(6.42±0.48) and (6.84±0.36) nmol/mg, respeetively;all: P <0.05]. The Na+ K+ ATPase and TAOC levels were significantly lower in all of the RS groups than those in the SS group (all: P < 0.05), and those in the RS80 and RS100 groups was significantly lower than those in the RS40,RS50 and RS60 groups (all: P <0.05). Blood perfusion in the RS80 and RS100 groups was significantly lower than that in the other groups (all: P < 0.05). Conclusions If hemorrhage is uncontrolled, limited resuscitation appears to balance the needs for organ perfusion, improve the microcircttlation and decrease lactate levels. Fur-thermore, limited resuscitation could decrease ischemia-reperfusion injury in liver tissue.     

限制性液体复苏对肝脏缺血-再灌注损伤的影响

Objective To investigate the effects of limited resuscitation on hepatic ischernia-reperfusion in-jury in rots with hemorrhagic shock. Method Uncontrolled hemorrhagic shock was induced in 54 rats by transect-ing the middle branch of the splenic artery to produce standardized massive splenic injury. Resuscitation started when the mean arterial pressure (MAP) reached 40 mmHg. The rats were randomly divided (n = 9per group) in-to sham-operated group (SS), or one of five treatment groups in which infusion of Ringer' s solution was continually administrated to maintain MAP at 40 (RS40), 50 (RS50), 60 (RS60), 80 (RS80) or 100 mmHg (RS100) for 45 minutes (T45 point). After the bleeding was controlled, resuscitation was continued with Ringer's solution and whole blood (2:1) to increase the MAP to 100 mmHg for 120 minutes (T165 point), which was followed by obser-vation for 240 minutes (T405 point). All animals were observed for 240 minutes or until death. Blood specimens were collected at TO, T45, T165 and T405 for determination of blood lactate levels. At the end of the experiment,a small amount of hepatic tissue was collected to measure tissue blood perfusion, total antioxidative capacity (TAOC), Na+K+ ATPase activity and malondialdehyde (MDA) levels. Results At T405, the blood lactate lev-els in the RS80 and RS100 groups [(3.60±0.68) and (3.84 ± 1.09) mmol/L, respectively] were significantly higher than those in the SS, RS40, RS50 and RS60 groups [(2.00±0.66),(2.74±1.45),(2.43 +0.94) and (2.07±0.95) mmol/L, respectively;all:P < 0.05]. The MDA levels were significantly higher in the RS80 and RS100[(7.32±0.31) and (7.71±0.23) nmol/mg,respectively] than those in the SS, RS40, RS50 and RS60 groups[(4.95±0.80),(6.14±0.94),(6.42±0.48) and (6.84±0.36) nmol/mg, respeetively;all: P <0.05]. The Na+ K+ ATPase and TAOC levels were significantly lower in all of the RS groups than those in the SS group (all: P < 0.05), and those in the RS80 and RS100 groups was significantly lower than those in the RS40,RS50 and RS60 groups (all: P <0.05). Blood perfusion in the RS80 and RS100 groups was significantly lower than that in the other groups (all: P < 0.05). Conclusions If hemorrhage is uncontrolled, limited resuscitation appears to balance the needs for organ perfusion, improve the microcircttlation and decrease lactate levels. Fur-thermore, limited resuscitation could decrease ischemia-reperfusion injury in liver tissue.