核因子-κB、IκB在创伤失血性休克大鼠肝损伤中的作用

目的 从组织受体水平探讨核因子-κB(NF-κB)、IκB在创伤失血性休克后肝组织中的变化及其在肝损伤中的作用机制.方法 雄性健康Wistar大鼠36只,采用双侧股骨骨折伴失血性休克模型,随机分成正常对照组6只,双侧股骨骨折伴失血性休克组30只.动态观察伤后0.5、2、4、6、8 h大鼠肝组织核因子-κB、IκB、肝脏病理、肝功能、TNF-α、IL-6等变化.肝组织NF-κB采用EMSA法测定结合活性、IκB采用免疫印迹法测定其蛋白含量,并进行计算机图像分析.数据采用SPSS 12.0软件分析,两组间比较采用配对资料的t检验.结果 NF-κB的活性伤后迅速升高,伤后2 h与正常对照相比,差异具有统计学意义,[(8.4±0.7) vs (2.3±0.4),P＜0.01];伤后6 h达到高峰,和正常组相比,P＜0.01[(43.4±4.6) vs (2.3±0.4),P＜0.01].IκB伤后迅速降低,伤后2 h和正常对照相比,差异具有统计学意义[(17.0±2.0) vs (26.4±2.2),P＜0.01].伤后6 h继续下降至比较低的水平,和正常组相比,P＜0.01[(6.5±1.1) vs (26.4±2.2),P＜0.01].TNF-α、IL-6伤后逐渐升高,并于伤后6 h达到高峰:和正常组相比,P＜0.01[TNF-α,(173.7±12.1) vs (30.8±1.8)pg/ml,P＜0.01;IL-6,(175.5±12.5) vs (10.4±0.7)pg/ml,P＜0.01].光镜下伤后4～8 h肝窦内有少许淤血,有散在炎性细胞浸润;血清ALT、TB伤后4 h开始增高,和正常组相比,P＜0.01[ALT,(640.6±80.2) vs (536.8±60.0)nmol·L-1,P＜0.01;TB,(4.7±1.1) vs (1.6±0.2)mol/L,P＜0.01];白蛋白伤后4 h明显下降,和正常组相比,P＜0.01[(13.3±1.6) vs (20.6±3.4)g/L,P＜0.01].结论 NF-κB及其抑制蛋白IκB参与了严重创伤失血性休克后肝损伤的发生;且NF-κB增高越多、IκB减少越明显,肝损害越重.提示NF-κB及其IκB在严重创伤休克后肝组织细胞损伤与抗损伤机制方面起着重要作用.     

抑制核因子-κB对创伤休克大鼠肝脏热休克蛋白70的影响

目的 探讨抑制核因子-κB(NF-κB)后热休克蛋白70(HSP70)在创伤失血性休克肝组织中的变化及其对肝脏结构和功能的影响.方法 雄性健康Wistar大鼠66只,采用双侧股骨骨折伴失血性休克创伤模型,随机分成正常对照组6只,创伤休克组30只,NF-κB抑制伴创伤休克组30只,NF-κB抑制采用致伤前1 h腹腔注射二硫代氨基甲酸吡咯烷(PDTC)200mg/kg.动态观察伤后0.5、2、4、6、8h大鼠肝组织NF-κB、HSP70、肝脏病理、肝功能、TNF-α、IL-6等变化.NF-κB采用EMSA法测定结合活性,HSP70采用免疫印迹法测定其蛋白含量,并进行计算机图像分析.数据采用SPSS 12.0软件分析,两组间比较采用成组资料的t检验.结果 NF-κB的活性伤后迅速升高,伤后6 h达到高峰;HSP70伤后2 h较正常对照相比[(10.8±1.1)、vs.(4.7±0.5),P＜0.01],伤后6 h达到高峰,和正常组相比[(23.0±1.7)vs.(4.7±0.5),P＜0.01].TNFα、IL-6伤后逐渐升高,并于伤后6 h达到高峰,和正常组相比[TNF-α(173.7±12.1)vs.(30.8±1.8)pg/ml,P＜0.01;IL-6(175.5±12.5)vs.(10.4±0.7)pg/ml,P＜0.01];伤后8 h光镜下可见肝窦内淤血明显,有大量炎性细胞浸润;血清ALT、TB伤后4 h开始增高,8 h达到峰值,和创伤组相比[ALT(640.6±80.2)vs.(536.8±60.0)nmol-1·L-1,P＜0.01;TB(4.7±1.1)vs.(1.6±0.2)mol/L,P＜0.01].抑制NF-κB再致伤后,HSP70在肝组织中表达仍然较高,但在伤后各个时相点的表达均较未抑制NF-κB创伤性休克伤组明显回落;伤后6 h和创伤组相比[(16.9±4.4)vs.(23.0±1.7),P＜0.05].TNF-α、IL-6伤后各个时相点均迅速回落,伤后6 h,和创伤组相比[TNF-α(135.2±10.2)vs.(173.7±12.1)pg/ml,P＜0.05;IL-6(113.0 4±10.8)vs.(175.5±12.5)pg/ml,P＜0.05];肝脏大体淤血、肿胀明显减轻;伤后8 h光镜下可见肝细胞变性明显好转,肝窦内淤血减轻,仅见少许淋巴细胞及中性粒细胞浸润;伤后4 h,血清ALT、TB即明显下降,和未抑制组相比[ALT(540.8±66.2)vs.(640.6±80.2)nmol-1·L-1,P＜0.05;TB(2.3±0.3)vs.(4.7±1.1)mol/L,P＜0.05].结论 NF-κB、HSP70参与了严重创伤失血性休克后肝损伤与抗损伤的发生,抑制NF-κB的活性有助于减轻创伤失血性休克后肝脏的急性损害,NF-κB、HSP70可作为反映创伤休克后肝脏损害程度的重要应激指标.     

糖皮质激素受体及核因子-κB在创伤休克大鼠肝脏中的作用

目的 探讨糖皮质激素受体(GR)、核因子-κB(NF-κB)在创伤失血性休克后肝组织中的变化、相互关系,及其对肝损伤的作用机制.方法 雄性健康Wistar大鼠96只,采用双侧股骨骨折伴失血性休克创伤模型,随机分成正常对照组6只,创伤休克组30只,GR阻断伴创伤休克组30只,NF-κB抑制伴创伤休克组30只.动态观察伤后0.5、2、4、6、8 h大鼠肝组织GR、NF-κB,肝脏病理,肝功能,血清TNF -α、IL-6等变化.GR采用免疫印迹法测定蛋白含量,NF-κB采用EMSA法测定结合活性,并进行计算机图像分析.结果 肝组织GR的蛋白含量在创伤失血性休克后2 h即开始下降,4 h明显低于正常对照(P<0.01),6 h降至最低,8 h仍显著低于正常(P<0.01);NF-κB的活性伤后迅速升高,伤后6 h达到高峰(P<0.01).光镜下伤后4～8 h肝窦内少许淤血,有散在炎性细胞浸润;血清TNF-α、IL-6、ALT、TB伤后4 h 开始增高.GR阻断后再致伤,NF-κB在伤后各个时相点的表达均较未阻断有明显增高,光镜下伤后2 h肝窦内即可见较多炎性细胞浸润,血清TNF-α、IL-6、ALT、TB在伤后2 h即有明显升高(P<0.01).抑制NF-κB再致伤后,GR在伤后肝组织中的表达增强,TNF-α、IL-6伤后各个时相点均迅速回落,光镜下伤后4～8 h肝细胞变性明显好转,肝窦内见淤血减轻,仅见少许淋巴细胞及中性粒细胞浸润;伤后4 h,血清ALT、TB即明显下降.结论 GR、NF-κB参与了严重创伤失血性休克后肝损伤的发生,阻断GR使NF-κB的表达增强,肝损害程度加重;抑制NF-κB使GR表达增加,肝损害程度减轻.提示GR及NF-κB在严重创伤休克后肝组织细胞损伤过程中关系密切并起着重要作用.     

不同液体复苏对失血性休克大鼠心肌核因子-κB表达的影响

目的 观察失血性休克大鼠心肌病理和核转录因子-κB(NF-κB)活性的变化以及不同液体复苏对其影响.方法 将40只Wistar大鼠,随机分为五组:假手术(Sham)组、休克(Shock)组、乳酸林格液复苏(RL)组、羟乙基淀粉复苏(HES)组、自身血液复苏(BL)组,每组8只,建立失血性休克再复苏大鼠模型.采集心脏组织,观察病理变化,并用免疫组化法检测NF-κB的表达情况.结果 与Sham组相比,其余各组心肌组织中NF-κB的表达均明显增加(P<0.05或P<0.01),且心肌有不同程度的损伤;BL组心肌NF-κB的表达增加明显低于RL、HES组(P<0.05),心肌损伤的程度也较轻.结论 不同液体复苏均可使失血性休克大鼠心肌组织NF-κB的表达和损伤程度明显降低,且二者呈显著正相关.自身血液与乳酸林格液和羟乙基淀粉相比,是较理想的失血性休克的复苏液体.     

不同方式液体复苏对失血性休克大鼠外周血单个核细胞中核转录因子-κB活性的影响

目的观察失血性休克大鼠外周血单个核细胞（PBMC）中核转录因子-κB（NF—κB）活性的变化以及不同方式液体复苏对其的影响。方法将32只成功复制的失血性休克模型SD大鼠随机分为对照组、无液体复苏组、限制性液体复苏组和快速大量液体复苏组，每组8只；比较各组的救治疗效，并用酶联免疫吸附法（ELISA）检测各组PBMC中NF—κB活性的变化。结果限制性液体复苏组大鼠的存活时间较快速大量液体复苏组及无液体复苏组明显延长（P均〈0．05）；限制性液体复苏组大鼠72h存活率明显高于快速大量液体复苏组和无液体复苏组，但低于对照组（P均〈0．05）。除对照组外，其余各组创伤后60min和120min PBMC中NF—κB活性均较创伤前有明显升高，且120min较60min也明显升高（P均〈0．05）；限制性液体复苏组NF～κB活性明显低于快速大量液体复苏组和无液体复苏组（P均〈0．05）；死亡组创伤后60min和120min NF—κB活性明显高于存活组（P均〈0．05）。结论限制性液体复苏可显著降低失血性休克大鼠的72h死亡率；PBMC中NF—κB活性与预后密切相关，NF—κB活性高则提示预后不良，而限制性液体复苏时NF-κB活性明显降低，有助于改善预后。     

地塞米松对脑损伤大鼠核转录因子-κB水平的影响

Objective To explore the effects of dexamethasone on nuclear factor-kB (NF-κB) expression in brain tissue after traumatic brain injury (TBI). Methods Forty rats were randomly divided into two groups: dexamethasone treatment and no treatment, and severe brain injury was produced by gas percussion in both groups. At 0, 6, 24, 72 and 120 hours after injury, 5 rats of each group were executed and the histopathological changes in brain tissue in rats were observed by hematoxylin-eosin (HE) stain. The expression of NF-κB in brain tissue of rats was detected by immunohistochemical method. Results NF-κB expression was significantly up-regulated at 6 hours in brain tissue of rats after TBI (P<0.05), reaching the highest level at 24 hours (P<0. 01). It showed a tendency to lower, but was still high at 120 hours after TBI (P<0. 05 or P<0. 01). After treatment with dexamethasone, NF-κB level was lowered at 6, 24 and 72 hours (all P<0. 01). Conclusion NF-κB expression is up-regulated in brain tissue in early period after TBI, and keeps on a high level, thus inducing inflammatory response to produce secondary injury to brain tissue. Dexamethasone shows protective effects by regulating the levels of NF-κB and prevents secondary injury which is caused by the inflammatory cytokines in rat brain tissue after TBI.     

地塞米松对脑损伤大鼠核转录因子-κB水平的影响

Objective To explore the effects of dexamethasone on nuclear factor-kB (NF-κB) expression in brain tissue after traumatic brain injury (TBI). Methods Forty rats were randomly divided into two groups: dexamethasone treatment and no treatment, and severe brain injury was produced by gas percussion in both groups. At 0, 6, 24, 72 and 120 hours after injury, 5 rats of each group were executed and the histopathological changes in brain tissue in rats were observed by hematoxylin-eosin (HE) stain. The expression of NF-κB in brain tissue of rats was detected by immunohistochemical method. Results NF-κB expression was significantly up-regulated at 6 hours in brain tissue of rats after TBI (P<0.05), reaching the highest level at 24 hours (P<0. 01). It showed a tendency to lower, but was still high at 120 hours after TBI (P<0. 05 or P<0. 01). After treatment with dexamethasone, NF-κB level was lowered at 6, 24 and 72 hours (all P<0. 01). Conclusion NF-κB expression is up-regulated in brain tissue in early period after TBI, and keeps on a high level, thus inducing inflammatory response to produce secondary injury to brain tissue. Dexamethasone shows protective effects by regulating the levels of NF-κB and prevents secondary injury which is caused by the inflammatory cytokines in rat brain tissue after TBI.     

地塞米松对脑损伤大鼠核转录因子-κB水平的影响

Objective To explore the effects of dexamethasone on nuclear factor-kB (NF-κB) expression in brain tissue after traumatic brain injury (TBI). Methods Forty rats were randomly divided into two groups: dexamethasone treatment and no treatment, and severe brain injury was produced by gas percussion in both groups. At 0, 6, 24, 72 and 120 hours after injury, 5 rats of each group were executed and the histopathological changes in brain tissue in rats were observed by hematoxylin-eosin (HE) stain. The expression of NF-κB in brain tissue of rats was detected by immunohistochemical method. Results NF-κB expression was significantly up-regulated at 6 hours in brain tissue of rats after TBI (P<0.05), reaching the highest level at 24 hours (P<0. 01). It showed a tendency to lower, but was still high at 120 hours after TBI (P<0. 05 or P<0. 01). After treatment with dexamethasone, NF-κB level was lowered at 6, 24 and 72 hours (all P<0. 01). Conclusion NF-κB expression is up-regulated in brain tissue in early period after TBI, and keeps on a high level, thus inducing inflammatory response to produce secondary injury to brain tissue. Dexamethasone shows protective effects by regulating the levels of NF-κB and prevents secondary injury which is caused by the inflammatory cytokines in rat brain tissue after TBI.     

地塞米松对脑损伤大鼠核转录因子-κB水平的影响

Objective To explore the effects of dexamethasone on nuclear factor-kB (NF-κB) expression in brain tissue after traumatic brain injury (TBI). Methods Forty rats were randomly divided into two groups: dexamethasone treatment and no treatment, and severe brain injury was produced by gas percussion in both groups. At 0, 6, 24, 72 and 120 hours after injury, 5 rats of each group were executed and the histopathological changes in brain tissue in rats were observed by hematoxylin-eosin (HE) stain. The expression of NF-κB in brain tissue of rats was detected by immunohistochemical method. Results NF-κB expression was significantly up-regulated at 6 hours in brain tissue of rats after TBI (P<0.05), reaching the highest level at 24 hours (P<0. 01). It showed a tendency to lower, but was still high at 120 hours after TBI (P<0. 05 or P<0. 01). After treatment with dexamethasone, NF-κB level was lowered at 6, 24 and 72 hours (all P<0. 01). Conclusion NF-κB expression is up-regulated in brain tissue in early period after TBI, and keeps on a high level, thus inducing inflammatory response to produce secondary injury to brain tissue. Dexamethasone shows protective effects by regulating the levels of NF-κB and prevents secondary injury which is caused by the inflammatory cytokines in rat brain tissue after TBI.     

地塞米松对脑损伤大鼠核转录因子-κB水平的影响

Objective To explore the effects of dexamethasone on nuclear factor-kB (NF-κB) expression in brain tissue after traumatic brain injury (TBI). Methods Forty rats were randomly divided into two groups: dexamethasone treatment and no treatment, and severe brain injury was produced by gas percussion in both groups. At 0, 6, 24, 72 and 120 hours after injury, 5 rats of each group were executed and the histopathological changes in brain tissue in rats were observed by hematoxylin-eosin (HE) stain. The expression of NF-κB in brain tissue of rats was detected by immunohistochemical method. Results NF-κB expression was significantly up-regulated at 6 hours in brain tissue of rats after TBI (P<0.05), reaching the highest level at 24 hours (P<0. 01). It showed a tendency to lower, but was still high at 120 hours after TBI (P<0. 05 or P<0. 01). After treatment with dexamethasone, NF-κB level was lowered at 6, 24 and 72 hours (all P<0. 01). Conclusion NF-κB expression is up-regulated in brain tissue in early period after TBI, and keeps on a high level, thus inducing inflammatory response to produce secondary injury to brain tissue. Dexamethasone shows protective effects by regulating the levels of NF-κB and prevents secondary injury which is caused by the inflammatory cytokines in rat brain tissue after TBI.     

核因子-κB在小鼠急性肺损伤中的作用

目的　探讨核因子 (NF) κB在内毒素 (LPS)诱导的急性肺损伤小鼠发病中的作用。方法　腹腔内注射LPS诱导小鼠急性肺损伤模型。LPS注射后 0、 1、 3、 6、 12测定肺湿重 /干重比值 (W/D) ,迁移率改变电泳法检测肺组织NF κB活性 ,同时酶联免疫吸附法测定肺组织匀浆中肿瘤坏死因子 (TNF) α、白介素 (IL) 10浓度 ,RT PCR检测mRNA表达。结果　LPS注射后 ,W/D比值明显增高 ,6h升高最明显 (4 82± 0 10 ) ,显著高于LPS注射前 (3 6 7± 1 0 4 ,P <0 0 5 )。LPS注射后肺组织核蛋白NF κB活性明显增强 ,6h达到峰值 (40 5 7± 6 2 4 ) ,显著高于LPS注射前 (44 8± 30 9,P <0 0 5 )。肺组织匀浆TNF α和IL 10浓度分别在LPS注射后 6h和 12h升高最明显 ,分别为 (197 1± 5 2 4 )pg/ml和 (6 4 9± 39 7)pg/ml,显著高于LPS注射前 [分别为 (6 1 2± 10 7)pg/ml和 (71 6± 15 9)pg/ml]。与LPS注射前比较 ,LPS注射后 3～ 12h ,肺组织匀浆TNF α和IL 10mRNA表达显著增高。肺组织病理显示肺泡出血、水肿、大量炎症细胞浸润 ,电镜下见Ⅰ型肺泡上皮细胞断裂 ,Ⅱ型肺泡上皮细胞变性。结论　LPS导致肺组织NF κB的活化 ,介导炎症介质大量表达 ,参与急性肺损伤发生     

缺血性脑损伤与核因子κB

目的：探讨核因子κB在脑缺血中的作用，明确抗核因子κB的治疗是否为缺血性脑血管病的较为理想的治疗方式。 资料来源：应用计算机检索Medline 1995-01／2005—12关于运动猝死的文章。检索词“cerebral isehemia，NF—κB”并限定文章的语种类为English。同时利用计算机检索中国期刊全文数据库2002—01／2004—12的相关文章，限定文章语言种类为中文，检索词“脑缺血，核因子κB”。 资料选择：选择关于核因子κB与脑缺血方面的文献，不排除其是否为随机、盲法等论证推荐的文章。 资料提炼：共收集到符合上述要求的文献85篇，排除20篇重复性研究。65篇符合纳入标准。 资料综合：脑缺血后核因子κB被激活，通过促进细胞因子、黏附因子及炎性酶的转录、诱导神经细胞凋亡、调节胶质细胞的活性、介导自由基损伤等来参与缺血性脑损伤。抗核因子κB的治疗可以有效地减轻缺血后脑组织损伤。 结论：脑缺血可诱导核因子κB的激活，核因子κB通过调控多种基因的表达参与了缺血后的炎症反应和神经元的凋亡，在缺血性脑损伤中起到重要作用。针对核因子κB作为治疗脑缺血损伤的靶点对有效防治脑缺血具有重要的理论和临床意义。     

缺血性脑损伤与核因子κB

目的:探讨核因子κB在脑缺血中的作用,明确抗核因子κB的治疗是否为缺血性脑血管病的较为理想的治疗方式。资料来源:应用计算机检索Medline1995-01/2005-12关于运动猝死的文章。检索词“cerebralischemia,NF-κB”并限定文章的语种类为English。同时利用计算机检索中国期刊全文数据库2002-01/2004-12的相关文章,限定文章语言种类为中文,检索词“脑缺血,核因子κB”。资料选择:选择关于核因子κB与脑缺血方面的文献,不排除其是否为随机、盲法等论证推荐的文章。资料提炼:共收集到符合上述要求的文献85篇,排除20篇重复性研究。65篇符合纳入标准。资料综合:脑缺血后核因子κB被激活,通过促进细胞因子、黏附因子及炎性酶的转录、诱导神经细胞凋亡、调节胶质细胞的活性、介导自由基损伤等来参与缺血性脑损伤。抗核因子κB的治疗可以有效地减轻缺血后脑组织损伤。结论:脑缺血可诱导核因子κB的激活,核因子κB通过调控多种基因的表达参与了缺血后的炎症反应和神经元的凋亡,在缺血性脑损伤中起到重要作用。针对核因子κB作为治疗脑缺血损伤的靶点对有效防治脑缺血具有重要的理论和临床意义。     

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.     

Increased susceptibility to liver injury after hemorrhagic shock in rats chronically fed ethanol: role of nuclear factor-kappa B, interleukin-6, and granulocyte colony-stimulating factor

Chronic ethanol use preceding severe trauma and hemorrhagic shock (HS) is associated with an increased incidence of multiorgan failure (MOF) and death; however, the molecular basis for this increased susceptibility is unknown. We previously demonstrated that production of interleukin-6 (IL-6) and granulocyte colony-stimulating factor (G-CSF), mediated by nuclear factor-kappa B (NF-kappa B), each make essential contributions to organ injury and inflammation in a rodent model of controlled HS, and we proposed in this study to examine the hypothesis that the increased susceptibility to MOF after shock/trauma in the setting of chronic ethanol use is due to an exaggerated activation of NF-kappa B and production of these proinflammatory cytokines. We observed increased HS-induced liver injury 4 h after resuscitation in rats fed the ethanol-containing Lieber-DeCarli liquid diet for 8 weeks compared with rats fed the control liquid diet (3-fold increase in serum alanine aminotransferase [ALT], P = 0.008, and 2-fold increase in focal liver necrosis, P = 0.005). The increased liver injury in the ethanol-fed HS rats was accompanied by a 70% increase in liver NF-kappa B activation (P < 0.05), a 3- to 5-fold increase in hepatocyte and Kupffer cell production of IL-6 and G-CSF (P < 0.05 for each), and a 2-fold increase in neutrophil infiltration (P < 0.005) compared with the control diet-fed HS rats. Thus, increased susceptibility to HS-induced liver injury in the setting of chronic ethanol use may be mediated, at least in part, by increased NF-kappa B activation resulting in increased local production of IL-6 and G-CSF and increased infiltration of neutrophils, which can damage liver cells directly and contribute to impaired sinusoidal blood flow.     

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.     

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.