肝部分切除+定容失血性休克大鼠肝脏cDNA表达谱芯片结果分析

目的 利用cDNA表达谱芯片分析肝部分切除+定容失血性休克前和休克后24小时大鼠肝脏差异基因,并初步分析差异基因信号通路和网络调控. 方法 11只大鼠接受肝左外叶切除和2.5ml/100g体重定容失血性休克,选其中3只存活大鼠麻醉后失血前切除肝左外叶(A组),对于存活24小时的大鼠再次取肝脏(B组)行cDNA表达谱芯片(含21793个基因)分析.对差异基因行Pathway、Go、Network分析.使用RT-PCR对两组中基因Aldh1a1、Aldh1a7、Aoc3、Cyp26a1、Hdc1、Ephx2和Beta-actin进行分析,验证cDNA芯片的准确性. 结果 4只大鼠存活24小时,表达谱芯片筛查出两组差异表达下调基因634个,表达上调基因513个.差异基因涉及主要信号通路包括胆固醇代谢、细胞外刺激反应、甾醇代谢、激素刺激反应、甾体类激素刺激反应、类固醇代谢、内源性刺激反应、氧化还原反应、有机物质反应、脂肪酸代谢.结论 氧化还原和脂代谢信号通路在创伤失血性休克病理过程中起重要作用.     

失血性休克急性肺损伤的发病机制

背景 急性肺损伤(acute lung injury,ALI)是失血性休克死亡率和发病率升高的重要原因. 目的 对失血性休克ALI的可能发病机制作一综述. 内容 多核中性粒细胞(polymorph nuclear neutrophils,PMNs),Toll样受体(Toll-like receptors,TLRs),活性氧(Reactive Oxygen Species,ROS),低氧诱导因子(hypoxia-inducibie factor,HIF)以及核因子(nuclear factor-κB,NF-κB)的激活和相互作用参与了创伤失血性休克后ALI,并且发挥了关键作用. 趋势 加深对创伤失血性休克ALI发病机制和各种损伤因素横向联系将有助于其治疗.     

Changes in brain monoamines and their metabolites during and after hemorrhagic shock in the rat

The alteration of monoamines and their metabolites in the brain during and after hemorrhagic shock in the conscious state was measured in rats. Blood pressure was maintained at 40–70mmHg (5.3–9.3kPa) for 60min by withdrawing 8ml of blood intermittently. The content of monoamines, as well as their metabolites, increased in various brain regions during hemorrhage, compared with the content in the control rats. Sixty min after the end of the bleeding period, almost no significant change in the contents of brain monoamines nor of their metabolites was observed. These results may indicate not only an increased release of monoamines from nerve terminals, but also an increased synthesis of them during hemorrhagic shock. Soon after the bleeding was stopped, the increased monoamine turnover rate returned to almost normal levels.(Mizobe T, Okuda C, Demura H et al.: Changes in brain monoamines and their metabolites during and after hemorrhagic shock in the rat. J Anesth 4: 116–122, 1990)     

The effect of aprotinin in a model of uncontrolled hemorrhagic shock

BACKGROUND: Aprotinin has been shown to promote clot formation through its antifibrinolytic activity, by inhibiting the plasmin-induced complement activation and by protecting the platelets adhesive surface receptors. It has been successfully used in cardiac and liver transplantation surgery. OBJECTIVE: To evaluate the effect of aprotinin in a model of uncontrolled intra-abdominal bleeding as a basis for its potential use in trauma patients. METHODS: Twenty rats were randomly divided into 2 groups. All animals were operated on and bleeding was induced by transecting 1 lobe of the liver. In the treatment group a single dose of 30,000 U/kg of aprotinin was administered 5 minutes after the injury. The animals were monitored for hemodynamic parameters, blood loss volume, and mortality rates. RESULTS: At 120 minutes from trauma induction a significant difference in mean blood pressure was observed: 67+/-22 mm Hg in the treatment group versus 53+/-28 mm Hg in the control group (P=.04). This difference remained consistent until the end of the experiment. Treatment with aprotinin also resulted in a tendency to an increased survival rate (P=.05) and increased mean survival time: 175+/-46 minutes as compared to 123+/-48 minutes in the controls (P=.027). CONCLUSIONS: Early administration of aprotinin resulted in temporary hemodynamic stabilization and prolonged survival in a model of uncontrolled bleeding. Further studies are needed to establish the possible use of aprotinin in the treatment of trauma patients.     

潘氏细胞在大鼠休克复苏后肠黏膜重建过程中的作用

目的 观察小肠潘氏细胞在大鼠失血性休克复苏后肠黏膜重建过程中的作用。方法 42只雄性Wistar大鼠建立失血性休克复苏模型,随机分为实验组(n=7)和对照组(n=35),实验组再分5组,分别于复苏后1、3、6、12、24h观察回肠黏膜的形态学改变、复苏前后潘氏细胞数量及形态变化特点及各时相电镜下潘氏细胞结构特点。结果 休克复苏后小肠黏膜明显损伤,集中表现于绒毛部分。复苏后3h为明显,6h后绒毛已开始修复,至24h肠黏膜表面细胞连续性已恢复。复苏后1h,回肠黏膜潘氏细胞计数明显减少(P＜0.05),3h降至最低(P＜0.05),6h后与对照组比较,差异无统计学意义(P＞0.05)。电镜下潘氏细胞表现肠内分泌细胞超微结构特征,核无凋亡改变。结论 失血性休克复苏后肠黏膜屏障早期受损,但具快速重建能力,潘氏细胞颗粒的合成和分泌可受缺血再灌注损伤的诱导。潘氏细胞对维持肠道黏膜防御机制具有重要的生理意义。     

多发性创伤伴失血性休克限制性液体复苏的疗效分析

目的评价多发性创伤伴失血性休克早期采用限制性液体复苏(LFR)的治疗效果,以提高治愈率。方法将50例多发性创伤伴失血性休克患者随机分为LFR组和积极液体复苏(AFR)组,采用两组不同复苏方式,对两组患者的血乳酸(LA)、剩余碱(BE)、输入液体量进行统计学分析,对比两组的临床疗效。结果采用两种不同复苏方式治疗后,血乳酸[手术开始时:(3.26±0.52)mmol/Lvs(5.71±0.58)mmol/L;术后3小时:(2.35±0.36)mmol/Lvs(3.87±0.24)mmol/L]和剩余碱[手术开始时:(-5.56±0.49)mmol/Lvs(-9.48±0.71)mmol/L;术后3小时:(-3.54±0.22)mmol/Lvs(-5.34±0.68)mmol/L],两组间差异具有统计学意义(P0.05)。限制液体复苏组输液量、死亡率比较积极液体复苏组差异具有统计学意义[(1075±259)mlvs(2568±360)ml;(14.5%vs35.4%),P均0.05)]。结论在出血未控制的情况下,早期限制性液体复苏在减少输液量的同时可维持重要脏器的血流灌注,减轻酸中毒,为后续救治创造条件,降低病死率。     

维生素C对失血性休克大鼠脏器功能的影响及机制研究

目的:探讨维生素C(Vit C)对失血性休克(hemorrhagic shock,HS)大鼠脏器功能的保护作用。方法:首先对16只雄性SD大鼠随机分为腹腔内注射生理盐水组(空白对照组,n=8)和Vit C组(V2 h组,100 mg/kg,n=8),用免疫组化方法检测空肠、肝脏、肺脏及肾脏中血红素加氧酶1(heme oxygenase-1,HO-1)的表达。其次,32只SD大鼠随机分为假手术组(n=8),休克模型组(HS 24 h组,n=8),休克加Vit C组(HSV 24 h组,HS+Vit C,n=8)和HO-1抑制组(HSVZ 24 h组,HS+Vit C+ZnPP,n=8)。HSV 24 h组在造模前30 min腹腔注射Vit C(100 mg/kg),HSVZ 24 h在HSV24 h处理方法的基础上腹腔注射HO-1抑制剂ZnPP(3 mg/kg),各组在造模后24 h取血清,检测器官功能指标丙氨酸转氨酶、天冬氨酸转氨酶、尿素氮、肌酐、乳酸脱氢酶及肌酸激酶的表达,取空肠、肝脏、肺脏及肾脏,制作病理切片并行HE染色,进行病理评分。结果:正常SD大鼠注射Vit C 2 h后,空肠、肝脏、肺脏及肾脏HO-1表达明显增高。与假手术组相比,失血性休克大鼠各个器官的组织病理损伤及评分和各器官功能指标均显著增高(P<0.05),预先给予VitC可显著减轻以上病理指标(P     

高晶体-高胶体渗透压混合液对失血性休克大鼠不同组织中血管紧张素原表达的影响

目的 研究高晶体—高胶体渗透压混合液(HHS)复苏失血性休克时不同组织中血管紧张素原(angiotensinogen，ANG)表达的变化，探讨组织中的肾素—血管紧张素系统(renin-angiotensin system，RAS)活性的变化。方法 选取成年SD大鼠30只，随机平均分为复方乳酸钠(LRS)组和HHS组。制作失血性休克动物模型，分别用LRS或HHS复苏。采用逆转录酶—多聚酶链反应(reverse-transcrlptase-polymerase chain reaction，RT—PCR)的方法半定量测定各组大鼠休克前、休克后和复苏后30min的下丘脑、垂体前叶、肾上腺中的ANG基因表达水平，采用β—actin为内对照。结果 失血性休克后各组织中ANG表达水平均明显升高。只有HHS可降低各组织中的升高的ANG的表达水平。结论 HHS可抑制失血性休克时组织中的RAS的激活。     

Small volume resuscitation with 3% hypertonic saline solution decrease inflammatory response and attenuates end organ damage after controlled hemorrhagic shock

Background

Recently, studies have been conducted examining the efficacy of 3% hypertonic saline solution (HS) for the treatment of traumatic brain injury; however, few studies have analyzed the effects of 3% hemorrhagic shock during hemorrhagic shock. The aim of this study was to test the potential immunomodulatory benefits of 3% hemorrhagic shock resuscitation over standard fluid resuscitation.

Methods

Wistar rats were bled to a mean arterial pressure of 35 mm Hg and then randomized into 3 groups: those treated with lactated Ringer's solution (LR; 33 mL/kg, n = 7), 3% HS (10 mL/kg, n = 7), and 7.5% HS (4 mL/kg, n = 7). Half of the extracted blood was reinfused after fluid resuscitation. Animals that did not undergo shock served as controls (n = 5). Four hours after hemorrhagic shock, blood was collected for the evaluation of tumor necrosis factor-α and interleukin-6 by enzyme immunoassay. Lung and intestinal samples were obtained for histopathologic analysis.

Results

Animals in the HS groups had significantly higher mean arterial pressure than those in the LR group 1 hour after treatment. Osmolarity and sodium levels were markedly elevated in the HS groups. Tumor necrosis factor-α and interleukin-6 levels were similar between the control and HS groups but significantly higher in the LR group (P < .05). The lung injury score was significantly higher in the LR group compared with the 7.5% HS and 3% HS groups (5.7 ± 0.7, 2.1 ± 0.4, and 2.7 ± 0.5, respectively). Intestinal injury was attenuated in the 7.5% HS and 3% HS groups compared with the LR group (2.0 ± 0.6, 2.3 ± 0.4, and 5.9 ± 0.6, respectively).

Conclusions

A small-volume resuscitation strategy modulates the inflammatory response and decreases end-organ damage after HS. Three percent HS provides immunomodulatory and metabolic effects similar to those observed with conventional concentrations of HS.     

组蛋白脱乙酰化酶抑制剂对失血性和感染性休克早期救治作用的研究进展

背景 休克早期的药物救治,一直普遍受到关注,近来组蛋白脱乙酰化酶抑制剂(histone deacetylase inhibitors,HDACI)因其突出的抗休克作用成为国际研究热点. 目的 回顾目前HDACI的临床应用方向和分类,讨论其作为抗失血性休克和感染性休克药物的突出优势以及作用机制. 内容 HDACI可通过抗细胞凋亡等多种途径,提高细胞对休克所致缺血/缺氧环境的耐受能力,改善失血性休克和感染性休克动物模型的预后. 趋向 HDACI已成为抗失血性休克和感染性休克研究的新方向,是提高休克早期生存率的新策略,也为休克的治疗提供了药物配合液体复苏的新途径.     

高原失血性休克大鼠相关急性肺损伤病变及发病机制

目的探讨高原失血性休克相关急性肺损伤(acute lung injury,ALI)病变及发病机制。方法雄性Wistar大鼠72只,体重280~320g,随机分为六组:假手术组(Sham组)、休克15min组(HS15组)、休克30min组(HS30组)、休克45min组(HS45组)、休克60min组(HS60组)和休克90min组(HS90组),每组12只。建立高原大鼠失血性休克模型后,Sham组麻醉置管后不予失血,仅观察90min即刻处死,其余五组分别按照15、30、45、60和90min观察终止时间窗维持于休克状态。光镜下观察肺组织病理变化,测定肺湿/干重比(W/D)、计算肺通透指数,同时测定肺组织髓过氧化物酶(MPO)、总超氧化物歧化酶(T-SOD)的活性和丙二醛(MDA)的浓度,采用ELISA法检测肺组织中TNF-α和IL-10的浓度。采用免疫组化法检测肺组织中claudin-3和claudin-4的表达和分布。结果与Sham组比较,休克造成不同程度的肺损伤,且与休克维持时间成正比。在休克15~30min,大鼠肺组织W/D、肺通透指数、MPO、MDA、TNF-α、T-SOD和IL-10的变化甚微,在此之后,随着时间的延长,肺W/D、肺通透指数、MPO活性、MDA浓度和TNF-α浓度明显升高,同时伴随SOD活性和IL-10浓度的明显下降(P0.05)。claudin-3和claudin-4在肺上皮细胞和内皮细胞处的表达明显错位并减少(P0.05)。结论高原环境下,遭受失血性休克的大鼠血流动力学在短时间代偿后,病变呈现螺旋式恶化。且随着休克的延续,大鼠体内炎性/抗炎、氧化/抗氧化稳态失衡,导致肺上皮细胞内claudin-3和claudin-4流失,呈现出急性肺损伤的表现。     

Acute effects of massive transfusion of a bovine hemoglobin blood substitute in a canine model of hemorrhagic shock

The capability of stroma-free hemoglobin solutions to act as a plasma expander with oxygen and carbon dioxide transport properties has encouraged the idea of their possible use in settings of massive blood loss. Using a canine hemorrhagic shock model (systolic arterial pressure ≤50 torr for 60 min), we evaluated the efficacy of an ultra-pure stroma-free bovine hemoglobin solution (PBHg) as a resuscitation fluid in hypovolemic and acidotic animals, using homologous blood (PRBC) and 10% human serum albumin (HSA) as control solutions. Following volume replacement, dogs were studied for 2 h under anesthesia and for 4 h subsequently while awake. Resuscitation with PBHg (30 ± 3 ml/kg) was able to restore stable hemodynamics and correct acidosis to an extent comparable to that in animals treated with PRBC. Additionally, oxygen transport was maintained at a higher level than that in dogs treated with HSA. Administration of PBHg in this shock model revealed no significant cardiopulmonary toxicity or adverse effects. These short-term results suggest that PBHg may be useful for effective resuscitation after major blood loss.     

DNA微阵矩分析人软骨细胞体外老化过程中基因表达水平的变化

目的 研究成人软骨细胞体外单层培养老化过程中基因表达水平的变化，初步探索人软骨细胞老化发生的可能机制。方法 取体外培养的第1代(P)至第4代(P4)人肋软骨细胞，观察细胞增殖率，阿利新兰(Alcian blue)法定量检测硫酸软骨素蛋白聚糖聚集体(aggrecan)中糖胺多糖(GAGs)含量，RT-PCR分析Ⅰ、Ⅱ型胶原及aggreean基因表达量，以观察人软骨细胞体外老化过程。并采用DNA微阵矩技术对P1及P4软骨细胞表达差异的基因进行比较分析，P1及P4人肋软骨细胞基因表达水平差异≥2倍时，被认为差异具有显著性。结果 P4软骨细胞从细胞增殖率，细胞中GAGs含量，Ⅱ型胶原及aggrecan基因表达量分析均明显低于P1软骨细胞(P＜0．01)。在1000点的含有原癌基因、抑癌基因、细胞凋亡、应激反应蛋白基因和免疫相关基因的芯片分析中，P1及P4间存在差异的基因共36个，其中在P4中下调的基因11个，主要为细胞外基质、生长因子转录因子等，而在P4中上升的基因共25个主要为蛋白酶类、炎症因子及凋亡相关基因等。结论 P4软骨细胞呈现老化特征，通过DNA微阵矩技术发现P4老化细胞中基质合成相关基因表达下降，而降解酶类基因表达上升，致细胞外基质减少。且细胞增殖有关基因表达的减少及凋亡因子的增加，老化细胞增殖率下降；     

体外培养过程中去分化的人软骨细胞基因表达谱的变化

目的研究体外单层培养对人软骨细胞去分化的基因谱的影响,从而筛选出与人软骨细胞去分化的相关基因。方法取体外培养的第一代（P1）功能良好的人肋软骨细胞为对照组,而体外培养至第四代（P4）去分化的软骨细胞为实验组,取mRNA分别用Cy3,Cy5荧光标记,制作cDNA探针,采用BiostarH-80s含8300点的基因芯片表达谱分析P1及P4软骨细胞表达差异的基因,采用GenePixPro3.0软件分析,P1及P4人肋软骨细胞基因表达水平差异≥2倍时,被认为差异有统计学意义,重复3次。结果在8300点的相关基因中,P1及P4间存在差异的基因共140个,占总数的1.6%,其中在P4去分化软骨细胞中上升的基因56个,其中9条为与胞外基质降解及代谢相关基因,8条与应激、炎性反应相关基因,10条为生长抑制和细胞凋亡相关基因。而在P4中下调的基因84个,其中12条为蛋白质合成和能量代谢相关基因,16条为细胞周期和有丝分裂相关基因,12条为细胞骨架蛋白和信号传导相关基因。结论P4去分化细胞中基因表达特征为细胞外基质代谢失调,表现为基质合成相关基因表达下降,而降解酶类基因表达上升,应激与炎性反应亢进,凋亡蛋白合成增加,细胞分裂能力下降及离子转运能力下降,与软骨细胞去分化的病理生理特征相符。     

外源性磷酸肌酸抗失血性休克兔心肌损伤作用的研究

目的研究磷酸肌酸对失血性休克家兔心肌缺血再灌注损伤的保护作用。方法新西兰大耳白兔20只,随机分为磷酸肌酸注射液治疗组（CP组）和生理盐水对照组（N组）,各10只。制作家兔失血性休克模型,监测血流动力学指标（MAP）;分别于休克前（T0）、休克60min（T1）、复苏30min（T2）、60min（T3）、120min（T4）5个时间点抽血检测心肌肌钙蛋白（IcTnI）和肌酸激酶（CK）,实验终点取心脏组织观察其病理学及超微结构的改变,检测心肌线粒体Na＋-K＋-ATP酶和Ca2＋-ATP酶活性,并用TUNEL法检测心肌细胞的凋亡。结果与N组比较,CP组心肌病理组织学改变程度较轻;CP组在复苏期各个时间点的CK值和cTnI值均明显减低（P〈0.05）;CP组家兔心肌线粒体中的Na＋-K＋-ATP酶和Ca2＋-ATP酶活力均明显升高;CP组心肌TUNEL阳性细胞明显减少（P〈0.05）。结论磷酸肌酸具有抗失血性休克所致的心肌再灌注损伤作用。     

Buccal partial pressure of carbon dioxide outweighs traditional vital signs in predicting the severity of hemorrhagic shock in a rat model

Background

Hemorrhagic shock (HS) is a leading cause of death in both military and civilian settings. Researchers have investigated different parameters as predictors of HS, but reached inconsistent conclusions. We hypothesized that buccal partial pressure of carbon dioxide (PCO₂) was a better predictor of HS than traditional vital signs.

Materials and methods

Twenty-four anesthetized Wistar rats were randomly divided into four groups: one control group (no bleeding) and three surgical groups (25%, 35%, and 45% blood loss). Hemorrhage was induced by withdrawing blood from the left femoral artery over a period of 30 min. After that, resuscitation was performed on animals in surgical groups using the Ringer lactate solution. Buccal PCO₂ was continuously measured by a newly designed sensor holder during the experiments. Traditional vital signs, cardiac output, base excess, and microvascular perfusion (MPF) were also measured or calculated.

Results

Buccal PCO₂ differed significantly among four groups beginning at 20 min, approximately 10 min earlier than the shock index and more earlier than the heart rate, systolic blood pressure, and mean arterial pressure. Buccal PCO₂ correlated well with cardiac index and the changes in MPF. The correlation coefficients with cardiac index, chest MPF, and upper-limb MPF for buccal PCO₂ were 0.781, −0.879, and −0.946, respectively. Besides, buccal PCO₂ showed a good value for predicting mortality. Furthermore, an approximate critical threshold of buccal PCO₂ was also identified for predicting the severity of HS.

Conclusions

Buccal PCO₂ was a noninvasive, sensitive indicator of HS than traditional vital signs and may help on-scene rescuers administer early treatment of injured patients.     

Effect of hypothermia on apoptosis in traumatic brain injury and hemorrhagic shock model

IntroductionThe neuroprotective mechanisms of therapeutic hypothermia against trauma-related injury have not been fully understood yet. In this study, we aimed to investigate the effects of therapeutic hypothermia on biochemical and histopathological markers of apoptosis using Traumatic brain injury (TBI) and hemorrhagic shock (HS) model.MethodsA total of 50 male albino-wistar rats were divided into five groups: Group isolated TBI, Group NT (HT + HS + normothermia), Group MH (HT + HS + mild hypothermia), Group MoH (HT + HS + moderate hypothermia) and Group C (control). Neurological deficit scores were assessed at baseline and at 24 h. The rats were, then, sacrificed to collect serum and brain tissue samples. Levels of Caspase-3,6,8, proteoglycan-4 (PG-4), malondialdehyde (MDA), and nitric oxide (NO) were measured in serum and brain tissue samples. Histopathological examination was performed in brain tissue.ResultsThere were significant differences in the serum levels of Caspase-3 between Group NT and Group C (p = 0.018). The serum levels of Caspase-6 in Group NT (0.70 ± 0.58) were lower than Group MH (1.39 ± 0.28), although the difference was not statistically significant (p = 0.068). There were significant differences in the brain tissue samples for Caspase-3 levels between Group NT and Group C (p = 0.049). A significant difference in the Caspase-8 brain tissue levels was also observed between Group NT and Group C (p = 0.022). Group NT had significantly higher scores of all the pathological variables (for edema p < 0.017; for gliosis p < 0.001; for congestion p < 0.003, for hemorrhage p < 0.011) than Group C.ConclusionOur study results suggest that hypothermia may exert its neuroprotective effects by reducing markers of apoptotic pathway, particularly Caspase-3 on TBI and HS.     

转录因子Egr-1在失血性休克复苏后肝脏损伤中的作用

目的研究转录因子Egr-1在失血性休克复苏（HS/R）后肝脏损伤中的作用.方法利用Egr-1野生型（WT）和基因封闭型（KO）小鼠复制失血性休克复苏模型.取肝组织,RT-PCR法测定肝组织中TNF-α、IL-6、G-CSF、ICAM-1 mRNA的表达变化.通过检测肝组织中MPO的含量、血清ALT水平和组织学检查,评估肝脏炎症细胞浸润和损伤程度.结果失血性休克2.5 h＋复苏4 h后,Egr-1 KO小鼠肝组织中TNF-α、IL-6、G-CSF、ICAM-1 mRNA的表达水平明显低于Egr-1WT组;Egr-1 KO组失血性休克复苏后肝组织炎性浸润和损伤程度减轻,表现为血清ALT水平低,肝组织中MPO含量低,病理损伤轻.结论本实验结果表明转录因子Egr-1参与了失血性休克复苏后肝脏炎症反应基因表达的调节,在失血性休克复苏后的肝脏损伤中起一定的作用.     

Superiority of acetate compared with lactate in a rodent model of severe hemorrhagic shock

Background

Recently, we have shown that the use of lactated Ringer's (LR) solution is inferior to pure Ringer's solution (RS) in treatment of severe hemorrhagic shock in rats. The present study was performed to evaluate whether this is a specific effect of lactate or also applies to another metabolizable anion, namely acetate.

Material and methods

We subjected male Wistar rats to hemorrhagic shock by dropping the mean arterial blood pressure to 25–30 mm Hg for 60 min, resuscitated with acetated Ringer's (AR) solution, LR solution, RS, or normal saline (NS) within 30 min, and further observed the animals for 180 min.

Results

Administration of AR solution prolonged median survival to 115 min compared with 50 min for resuscitation with LR solution or 85 and 90 min for NS and RS, respectively. Resuscitation with AR solution and LR solution clearly improved metabolic acidosis compared with NS and RS but tissue injury, indicated by plasma enzyme activities, was most pronounced in the LR solution group, medium in the NS and RS groups, and least in the AR solution group.

Conclusions

In severe hemorrhagic shock, resuscitation with both RS and NS is superior to administration of LR solution but initial outcome is even further improved if AR solution is used. Mere amelioration of the acid–base status by AR solution may explain its superior role compared with RS and NS but cannot be responsible for its superiority compared with LR solution. Here, direct injury by lactate has to be discussed.