心肺复苏后组织因子和组织因子途径抑制物的动态变化和临床意义

目的 观察院内心肺复苏后不同时间点组织因子(TF)和组织因子途径抑制物(TFPI)水平的动态变化特点并探讨其临床意义.方法 选择2005年9月至2007年9月温州医学院附属第一医院急诊科收治的年龄>16岁明确心搏停止时间的心肺复苏患者24例,依据是否达到自主循环恢复标准随机分为ROSC和末ROSC两组,分别记录小同患者心搏停止的病因和临床特点,并用ELISA方法 检测心肺复苏(CPR)后30 min,60 min,6 h,24 h,48 h血清TF和TFPI抗原浓度,10例来自健康体检的健康自愿者为对照组.计量数据用均数±标准差((-x)±s)来表示,两组计量数据的比较采用独立样本t检验,三组及以上计量数据比较采用单因素方差分析法,计数数据的比较采用旧格表精确x2榆验,以P<0.05为差异具有统计学意义.结果 与对照组比较,ROSC组患者在CPR 30 min血TF水平显著升高(P<0.01),在CPR 6 h达高峰,在CPR48 h时已下降;与对照组及ROSC组同时点比较,末ROSC组血TF水平更是显著升高(P<0.01).与对照组比较,在CPR后30 min,ROSC和未ROSC两组血清TFPI水平差异无统计学意义(P>0.05),60 min后ROSC组血清TFPI水平逐渐升高并有显著差别(P<0.01或<0.05).与对照组比较,未ROSC组和ROSC组患者在CPR 30 min时的TF/TFPI水平均显著性升高(P<0.01),且前者显著高于后者(P<0.01),在ROSC组IF/TFPI值在CPR后6 h有显著升高(P<0.01),在48 h下降.结论 血清TF和TFPI水平在院内心肺复苏的患者中明显升高,CPR后半小时的TF和TF/TFPI的水平可用于判断预后.     

银杏达莫注射液对大鼠心肺复苏后血清低氧诱导因子-1α水平变化的影响

目的 观察大鼠心肺复苏(CPR)后血清低氧诱导因子-1α(HIF-1α)含量及大脑皮质的病理变化,探讨银杏达莫注射液对大鼠CPR后脑损伤的干预作用.方法 将160只成年雄性SD大鼠随机分为对照组、模型组、银杏达莫组低剂量组(0.8 ml/kg)、银杏达莫高剂量组(1.6 ml/kg),每组再分别按气管切开后(对照组)或自主循环恢复(ROSC)后(其余各组)0.5、3、6、9和24 h分为5个亚组,每个亚组8只大鼠.建立大鼠窒息型心脏停搏(CA)与CPR模型.以酶联免疫吸附法(ELISA)测定血清HIF-1α含量,光镜下观察大脑皮质病理改变.结果 对照组血清HIF-1α含量复苏后一直维持在较低水平;与对照组比较,模型组和银杏达莫高、低剂量组从ROSC后3 h起即显著升高,并持续至24 h,差异均有统计学意义(P均<0.01);与模型组比较,银杏达莫高、低剂量组血清HIF-1α含量于ROSC 3～24 h显著降低,且高剂量组降低幅度更为显著(P<0.05或P<0.01).银杏达莫高、低剂量组大脑皮质病理改变较模型组明显减轻.结论 大鼠CPR早期存在明显的脑损伤;银杏达莫注射液能明显减轻复苏后脑损伤,且该作用可能具有量效关系.     

脑出血患者血浆组织因子和组织因子途径抑制物含量变化及其意义

探测脑出血患者血浆组织因子及组织因子途径抑制物水平变化及其意义。以酶联免疫吸附测定（ＥＬＩＳＡ）法测定了脑出血患者的血浆组织因子（ＴＦ）和组织因子途径抑制物（ＴＦＰＩ）。结果：脑出血急性期患者血浆ＴＦ抗原和ＴＦＰＩ抗原明显高于正常人（Ｐ＜０．０１），而ＴＦＰＩ／ＴＦ比值降低；而恢复期患者ＴＦ与ＴＦＰＩ抗原水平以及ＴＦＰＩ／ＴＦ比值与正常人差异无显著意义。提示：急性期脑出血患者有血液高凝倾向。     

组织因子途径抑制物的临床研究进展

组织因子途径抑制物(tissue factor pathway inhibjtor,TFPI)是组织因子诱导的凝血过程的负性调节物之一。TFPI主要由微血管内皮细胞合成,可直接抑制因子Xa,并与因子Xa结合反馈抑制因子Ⅶa/组织因子复合物。在许多疾病诸如播散性血管内凝血(DIC)、缺血性心脏病、糖尿病、肝肾功能衰竭、晚期癌症等皆有升高,并在一定程度上与疾病的严重程度与预后相关。此外,随着重组TFPI的成功制备、动物实验的肯定结果及研究工作的不断完善,其在DIC、抗凝、溶栓和血     

急性冠状动脉综合征患者血浆组织因子及组织因子途径抑制物的变化及意义

急性冠状动脉综合征（ACS）是基于粥样斑块的破裂而启动一系列事件并导致血栓形成。凝血过程的激活在血栓形成中起重要作用。为进一步了解组织因子(TF)和组织因子途径抑制物(TFPI)在ACS中的作用，我们测定了63例ACS即不稳定性心绞痛(UAP)及急性心肌梗死(AMI)患者的血浆TF和TFPI含量及活性，并探讨其临床意义。     

组织因子和组织因子途径抑制物与脓毒症

脓毒症的发生发展过程与炎症反应、凝血及抗凝过程和免疫功能紊乱等密切相关。由组织因子（TF）所启动的外源性凝血途径不仅在脓毒症凝血反应中起关键作用，而且在炎症反应中也起着重要的作用。而组织因子途径抑制物（TFPI）则为外源性凝血过程的重要负性调节物。研究表明，TF和TFPI与脓毒症关系密切。现就TF、TFPI在脓毒症中的作用进行综述。     

脐静脉内皮细胞组织因子及其抑制物表达中银杏内酯B的干预效应

目的:观察银杏内酯B在氧化低密度脂蛋白诱导的脐静脉内皮细胞组织因子及其抑制物表达中的干预作用。方法:实验于2005-08/12在中国协和医科大学基础医学院病理生理学系实验室进行。采用Ⅰ型胶原酶消化分离脐静脉内皮细胞,进行原代培养至2～4代。实验分组如下:①正常对照组。②氧化低密度脂蛋白刺激组(60mg/L,氧化低密度脂蛋白作用12h)。③银杏内酯B 氧化低密度脂蛋白刺激组(预先给予20,40,80,100mg/L的银杏内酯B作用1h后,再给予60mg/L氧化低密度脂蛋白作用12h)。每组实验重复3次。分别采用发色底物法和RT-PCR技术检测脐静脉内皮细胞中组织因子和组织因子途径抑制物蛋白活性及mRNA水平的变化。结果:正常对照组脐静脉内皮细胞组织因子表达量很低,氧化低密度脂蛋白刺激脐静脉内皮细胞12h后,组织因子蛋白活性[(17.770±1.721),(2.352±0.240)U/mL,P<0.05]及mRNA水平(1.21±0.06,0.32±0.03,P<0.05)明显升高,银杏内酯B可呈剂量依赖性地抑制组织因子蛋白活性升高;组织因子途径抑制物的变化与组织因子相反,氧化低密度脂蛋白作用脐静脉内皮细胞12h后,组织因子途径抑制物蛋白活性及mRNA水平分别比对照组降低了33.8%和64.2%,但预先给予不同浓度的银杏内酯B,对组织因子途径抑制物的表达无显著影响。结论:银杏内酯B呈剂量依赖性抑制氧化低密度脂蛋白诱导的脐静脉内皮细胞组织因子蛋白活性和mRNA的表达,但对氧化低密度脂蛋白所致组织因子抑制物蛋白活性和mRNA水平的降低无显著影响。     

急性心肌梗死患者组织因子及组织因子途径激活抑制物水平的变化

目的探讨急性心肌梗死(AMI)患者组织因子(TF)及组织因子途径激活抑制物(TF-PI)的变化及临床意义。方法用ELISA法分别检测50例AMI患者及20例健康对照的外周血TF及TFPI的抗原水平。比较15例支架手术患者冠状窦内及外周血的TFPI水平。比较并发糖尿病和/或高脂血症AMI患者与无并发症者的TFAg及TFPIAg水平。结果AMI患者的TFAg及TFPIAg较正常人均明显升高(P<0.01);支架患者冠状窦内的TFPI水平明显低于其外周血(P<0.01);有并发症患者的TF及TFPI水平均明显高于无并发症患者(分别为P<0.01和P<0.05)。结论AMI患者外周血凝血活性增高,并发糖尿病和/或高脂血症AMI患者的凝血活性较无并发症患者高,血栓形成使冠状动脉腔内的TFPI消耗而降低。     

不同治疗方法对急性心肌梗死患者血浆组织因子及组织因子途径抑制物的影响

目的 观察急性心肌梗死(AMI)患者血浆组织因子(TF)、组织因子途径抑制物(TFPI)水平的变化及不同治疗方法对血浆TF、TFPI的影响,探讨其意义.方法 将80例AMI患者依治疗方案不同分为介入治疗组(40例)和药物(低分子肝素)治疗组(40例),在两组患者入院时及治疗后6 h、24 h、1周采集外周静脉血,以ELISA法测定TF、TFPI水平,分析其动态变化,并以20名健康人作为对照组.结果 AMI患者血浆TF和TFPI水平均高于正常对照组(P<0.01),介入治疗组术后6 h血浆TF水平略有升高,之后出现下降,至术后1周仍高于治疗前(P<0.05);药物治疗组用药后TF 水平呈明显逐渐下降趋势;AMI患者血浆TFPI水平于治疗后均出现升高(P<0.05,P<0.01),且以药物治疗组更显著.结论 AMI发生时TF途径被启动,TFPI随之激活,抑制TF诱发的凝血过程,低分子肝素抗凝治疗较单纯急诊介入治疗促进TFPI发挥抗外源性凝血效果更明显.     

正常足月产妇及胎盘早剥产妇中组织因子和组织因子途径抑制物的研究

目的检测正常足月妊娠胎盘、蜕膜中组织因子（TF）和组织因子途径抑制物（TFPI）含量,探讨两者在产科凝血中的作用;检测正常足月产妇及胎盘早剥产妇母血及脐血中的TF、TFPI含量,探讨其对凝血和产妇并发症发生情况的影响。方法分别检测38例正常足月妊娠产妇的血浆、胎盘、蜕膜中TF、TFPI含量;同时检测38例正常孕产妇及28例胎盘早剥产妇分娩前24h内血液及分娩即刻脐血中的TF、TFPI含量。结果正常足月妊娠胎盘、蜕膜中的TF含量均显著高于血浆中的含量,胎盘中的TFPI含量显著低于血浆中的含量,差异有统计学意义（P〈0．05）;胎盘早剥产妇的血浆TF含量、脐血中的TF含量显著高于正常分娩产妇,差异均有统计学意义（P〈0．05）;胎盘早剥产妇的血浆TFPI含量、脐血中的TFPI含量显著低于正常分娩产妇,差异均有统计学意义（P〈0．01）;胎盘早剥产妇母血、脐血中TFPI／TF比值均显著低于正常分娩产妇,差异有统计学意义（P〈0．01）。结论TF和TFPI是体内重要的凝血和抗凝血因子,在产科凝血工作中发挥重要作用。     

Disposition of tissue factor pathway inhibitor during cardiopulmonary bypass

BACKGROUND: The tissue factor (TF) factor (F) VIIa complex activates coagulation FIX and FX to initiate coagulation, and also cleaves protease activated receptors (PARs) to initiate inflammatory processes in vascular cells. Tissue factor pathway inhibitor (TFPI) is the only specific inhibitor of the TF-FVIIa complex, regulating both its procoagulant and pro-inflammatory properties. Upon heparin infusion during cardiopulmonary bypass (CPB), a heparin releasable pool of endothelial associated TFPI circulates in plasma. Following protamine neutralization of heparin, the plasma TFPI level decreases, but does not return completely to baseline, suggesting that during CPB a fraction of the plasma TFPI becomes heparin-independent. We have investigated the structural and functional properties of plasma TFPI during CPB to further characterize how TFPI is altered during this procedure. METHODS: We enrolled 17 patients undergoing first-time cardiac surgery involving CPB. Plasma samples were obtained at baseline, 5 min and 1 h after start of CPB (receiving heparin), 10 min after protamine administration (off CPB) and 24 h following surgery. Samples were analyzed for full-length and free (non-lipoprotein bound) TFPI antigen by enzyme-linked immunosorbent assay (ELISA) and for TFPI anticoagulant activity using an amidolytic assay. Western blot analysis was used to identify TFPI species of varying molecular weights in three additional patients. Dunnett's test for post hoc comparisons was used for statistical analysis. RESULTS: The ELISA and Western blot data indicated that an increase in full-length TFPI accounted for most of the heparin releasable TFPI. Following heparin neutralization with protamine, the full-length TFPI antigen returned to baseline levels while the free TFPI antigen and the total plasma TFPI activity remained elevated. This was associated with the appearance of a new 38 kDa form of plasma TFPI identified by Western blot analysis. The 38 kDa form of TFPI did not react with an antibody directed against the C-terminal region of TFPI indicating it has undergone proteolysis within this region. All TFPI measurements returned to baseline 24 h following CPB. CONCLUSIONS: During CPB the full-length form of TFPI is the predominant form in plasma because of its prompt release from the endothelial surface following heparin administration. Upon heparin neutralization with protamine, full-length TFPI redistributes back to the endothelial surface. However, a new 38 kDa TFPI fragment is generated during CPB and remains circulating in plasma, indicating that TFPI undergoes proteolytic degradation during CPB. This degradation may result in a decrease in endothelium-associated TFPI immediately post-CPB, and may contribute to the procoagulant and proinflammatory state that often complicates CPB.     

银杏达莫注射液对大鼠肝缺血再灌注损伤的保护作用机制研究

目的探讨银杏达莫注射液(Gin)对大鼠肝缺血再灌注损伤的保护作用机制。 方法选取36只Wistar实验大鼠，按随机数字表法分为正常组(N组)、肝缺血再灌注模型组(M组)和银杏达莫注射液干预组(T组)，每组12只，M组、T组采用夹闭肝固有动脉1 h再灌注1 h的方法模拟大鼠肝缺血再灌注模型。T组造模前1周开始每日按3.6 ml/kg腹腔注射Gin，N、M组造模前1周开始每日注射同量生理盐水。采用苏木精-伊红(HE)染色检测肝组织细胞形态，Masson染色和天狼星红染色检测肝组织胶原纤维；免疫印迹(Western blot)检测肝组织B细胞淋巴瘤/白血病-2(Bcl-2)，Bcl-相关X蛋白(Bax)、Smad和蛋白激酶B(Akt)的蛋白表达水平；聚合酶链式反应(PCR)检测肝组织中Bax、Bcl-2、Smad和Akt mRNA表达水平；免疫组织化学检测肝组织中Bax、Bcl-2、白介素6(IL-6)和IL-10的表达情况，以及检测血清中超氧化物歧化酶(SOD)和丙二醛(MDA)水平。 结果HE染色显示，M组肝组织细胞损伤严重且炎症细胞多、细胞水肿明显；Masson和天狼星红染色表明，M组胶原纤维沉积较N组明显；3种染色结果均显示，T组肝组织炎性浸润、胶原纤维沉积程度均较M组轻。Western blot结果发现，以β-actin为内参，M组Bax、Bcl-2蛋白相对表达量(0.91±0.28，0.68±0.24)高于N组(0.22±0.19，0.23±0.12)(均P<0.01)，T组Bax蛋白相对表达量(0.48±0.11)低于M组(P<0.01)，Bcl-2蛋白相对表达量(0.89±0.25)高于M组(P<0.01)；以GAPDH为内参，M组Akt、Smad蛋白相对表达量(0.72±0.34，1.03±0.13)高于N组(0.17±0.09，0.57±0.26)(均P<0.01)，T组Akt蛋白相对表达量(1.47±0.89)高于M组(P<0.01)，Smad蛋白相对表达量(0.62±0.42)低于M组(P<0.01)。PCR结果显示，M组Bax、Bcl-2、Akt和Smad mRNA表达水平(0.76±0.03，0.55±0.06，0.96±0.09，1.58±0.16)均高于N组(0.29±0.04，0.36±0.05，0.64±0.06，0.53±0.14)(均P<0.01)，T组Bax和Smad mRNA表达水平(0.36±0.04，1.05±0.26)低于M组(均P<0.01)，Bcl-2和Akt mRNA表达水平(0.85±0.04，1.46±0.19)高于M组(均P<0.01)。免疫组织化学结果显示，M组Bax、Bcl-2、IL-6、IL-10阳性表达面积[(39.52±0.78)%，(4.62±0.94)%，(38.04±3.11)%，(6.48±1.14)%]均高于N组[(0.99±0.13)%，(0.96±0.12)%，(0.46±0.06)%，(0.47±0.17)%](均P<0.01)；T组Bax、IL-6阳性表达面积[(8.18±1.22)%，(6.05±0.92)%]低于M组(均P<0.01)，Bcl-2、IL-10阳性表达面积[(48.13±2.65)%，(31.91±4.86)%]高于M组(均P<0.01)。与N组SOD、MDA水平[(274.81±10.42)U/ml，(2.25±0.51)nmol/ml]相比，M组SOD水平[(113.24±8.52)U/ml]下降，MDA水平[(5.19±0.99)nmol/ml]升高(均P<0.01)。T组SOD水平[(221.51±6.25)U/ml]高于M组(P<0.01)，MDA水平[(3.91±0.86)nmol/ml]低于M组(P<0.01)。 结论银杏达莫注射液预处理可能通过PI3K/Akt和TGF-β/Smad信号通路介导的抑制细胞凋亡和纤维化发挥对大鼠肝缺血再灌注损伤的保护作用。     

硫酸镁对大鼠心肺复苏后神经功能恢复的影响

目的 探讨硫酸镁对大鼠室颤性心脏骤停心肺复苏模型的脑保护作用及其对血浆皮质醇浓度的影响.方法 30只SD雄性大鼠随机分为假手术组、心肺复苏模型组和复苏后硫酸镁干预组,每组10只.采用经食管电击法建立室颤性心脏骤停模型,改良的神经功能评分法测定神经功能,血浆皮质醇浓度用放射免疫法测定.结果 模型组和干预组在复苏后10 h神经功能评分均低于假手术组(P均<0.05),但模型组与干预组比较差异无统计学意义(P>0.05).模型组和干预组在复苏后10 h血浆皮质醇浓度均高于假手术组(P均<0.05),而模型组与干预组比较差异无统计学意义(P>0.05).结论 应用硫酸镁并不能改善室颤性心脏骤停心肺复苏模型大鼠复苏后10 h的脑神经功能,也未发现硫酸镁影响大鼠复苏后的血浆皮质醇浓度.     

心肺复苏后大鼠脑红蛋白变化及氯化血红素的作用

目的 观察心肺复苏(CPR)后大鼠脑皮质脑红蛋白(NGB)表达、神经功能评分(NDS)、大脑皮质病理的变化及氯化血红素(Hemin)干预的影响.方法 成年雄性SD大鼠120只,随机(随机数字法)分为3组(n=40):对照组(A)、复苏组(B)、药物组(C),建立窒息致大鼠心搏骤停CPR模型,观测大鼠自主循环恢复(ROSC)后各时间点(0.5 h,3 h,6 h,12 h,24 h)NGB表达、NDS及大脑皮质病理改变.实验数据作单因素方差分析,组间比较用Tukey检验.结果 与A组同时间点比较,B组ROSC后12 h,24 h NGB表达显著升高(P＜0.05或P＜0.01),ROSC后各时间点NDS显著降低(P＜0.01)、脑组织形态学明显异常;C组ROSC后6 h,12 h,24 h NGB表达显著升高(P＜0.05或P＜0.01),ROSC后3 h,6 h,12 h NDS显著降低(P＜0.01).与B组同时间点比较,C组ROSC后12 h,24 hNGB表达和NDS均显著升高(P＜0.01),ROSC后脑组织形态学异常明显减轻.结论 大鼠CPR后大脑皮质区NGB表达增加、NDS降低、脑组织形态学明显异常,Hemin能增加大脑皮层NGB表达、提高NDS、减轻皮层病理损伤,具有一定的脑保护作用.     

Effects of Hemin on neuroglobin expression after cardiopulmonary resuscitation in rats

BACKGROUND:

Despite a large amount of resuscitation research, the survival rate after cardiac arrest remains low, and brain injury is the key issue. Neuroglobin (NGB) is an oxygen-binding heme protein found in the brain with a protection role against ischemic-hypoxic brain injury. Hemin is an effective activator of neuroglobin. This study was undertaken to assess the effect of hemin on expression of neuroglobin (NGB) in the cerebral cortex, neuro-deficit score (NDS) and pathological changes after cardiopulmonary resuscitation (CPR) in rats.

METHODS:

A total of 120 male Sprague-Dawley (SD) rats were randomly divided into a control group (A), a CPR group (B) and a Hemin group (C). The animal model of cardiac arrest (CA) induced by asphyxia and CPR was established. NGB expression in the cerebral cortex with immunohistochemistry, NDS and pathological changes in the cerebral cortex were examined at 3, 6, 12, 24 hours after recovery of spontaneous circulation (ROSC) in each group. Experimental data were treated as one-factor analysis of variance and the Tukey test.

RESULTS:

In comparison with group A, NGB expression was increased significantly at 12 and 24 hours after ROSC (P<0.05 or P<0.01), NDS was decreased significantly at each time point after ROSC (P<0.01), and pathological changes were severe at each time point after ROSC in group B. In comparison with group A, NGB expression was increased significantly at 6, 12, 24 hours after ROSC (P<0.05 or P<0.01), NDS was decreased significantly at 3, 6, 12 hours after ROSC (P<0.01) in group C. In comparison with group B, NGB expression was increased significantly at 12 and 24 hours after ROSC, NDS was increased significantly at 12 and 24 hours after ROSC, and pathological changes were milder in group C.

CONCLUSION:

There were increased NGB expression in the cerebral cortex, decreased NDS, and severe pathological changes after CPR in rats. Hemin treatment up-regulated expression of NGB, improved NDS, mitigated pathological changes, and alleviated cerebral injury after CPR.KEY WORDS: Cardiopulmonary resuscitation, Neuroglobin, Neurodeficit score, Hemin, Cerebral injury, Rats     

Imbalance between tissue inhibitor of metalloproteinase 1 and matrix metalloproteinase 9 after cardiopulmonary resuscitation

Aims

This study aimed to determine whether (a) there was an imbalance between matrix metalloproteinase 9 (MMP-9) and tissue inhibitor of metalloproteinase 1 (TIMP-1) after cardiopulmonary resuscitation (CPR) in a canine model of prolonged ventricular fibrillation (VF); (b) with the duration of VF, the degree of the imbalance would be greater; and (c) there was a relationship between the level of MMP-9 or TIMP-1 and the cardiac function.

Methods and Results

Ventricular fibrillation was electrically induced in 24 dogs. The animals were randomly divided into 3 groups (sham control, n = 8; 8-minute VF, n = 8; 12-minute VF, n = 8). Echocardiographic measurement and hemodynamic variables were recorded before VF and after return of spontaneous circulation. Tissue inhibitor of metalloproteinase 1 (TIMP-1) and MMP-9 were analyzed by Western blot and immunohistochemistry. Compared with sham controls, dogs under VF and CPR showed significantly decreased level of TIMP-1 (P < .001), and with the duration of VF, the level of TIMP-1 declined (P < .01). The level of MMP-9 did not achieve statistical significance in the 3 groups (P > .05); however, they were higher in VF and longer duration VF groups. The ratios of TIMP-1/MMP-9 were lower in VF groups (P < .05). There was a negative correlation between TIMP-1 and left atrium dimension and left ventricular diastolic dimensions (r = −0.83 and r = −0.96, respectively; P < .01) and a positive correlation between TIMP-1 and left ventricular ejection fraction (r = 0.85; P < .01).

Conclusions

There was an imbalance between TIMP-1 and MMP-9 after CPR. It may partly contribute to the postresuscitation cardiac dysfunction.     

黄芪抑制心肺复苏后大鼠肝细胞凋亡的实验研究

目的研究黄芪注射液对心肺复苏后的大鼠肝细胞凋亡的抑制作用。方法SD雄性大鼠30只,随机分为5组:对照组、实验组(复苏后6h、24h)、黄芪组(复苏后6h、24h),每组6只。采用细胞凋亡原位末端标记法并结合透射电镜观察,分别检测各组大鼠肝细胞凋亡及Bcl2、Bax、NFκB的阳性表达。结果在各组大鼠肝组织内均可见肝实质细胞凋亡现象,实验组肝细胞TUNEL阳性表达率6h组为(56.63±3.41)%,24h组为(47.53±2.15)%,黄芪组的TUNEL阳性表达率6h组为(38.26±3.0)%,24h组为(28.59±2.31)%,对照组的TUNEL阳性表达率为(3.12±0.56)%;黄芪组Bel2、NFκB的表达高于实验组,而Bax的表达低于实验组。结论黄芪注射液对心肺复苏后大鼠肝细胞凋亡有保护作用。