内毒素休克时细胞膜脂流动性的改变及其机理探讨

用大肠杆菌内毒素致兔感染性休克模型，研究兔红细胞膜和／或肝、肺、心、肾线粒体膜磷脂酶Ａ２（ＰＬＡ２）活性，脂质过氧化产物丙二醛（ＭＤＡ）含量与膜脂流动性的变化及其可能的机理。动物随机分为休克组（ｎ＝１０）和对照组（ｎ＝１０）。取休克前、后１ｈ、３ｈ和５ｈ动脉血制备红细胞膜悬液；休克后８ｈ活杀动物（或死亡即刻）取肝、肺、心、肾组织制备线粒体膜悬液。内毒素休克后ＰＬＡ２活性和ＭＤＡ含量显著高于伤前和对     

不同缺血方式对大鼠肾脏损伤作用的实验研究

目的 研究在总缺血时间一定的情况下不同缺血方式对肾脏的损伤程度及其作用机理。方法 ４５只Ｗｉｓｔａｒ大鼠制备成肾缺血动物模型。Ａ组为正常对照组（ｎ＝１０）;Ｂ组为持续缺血组（ｎ＝１０）;Ｃ组为间断缺血组（ｎ＝１０）;Ｄ组为缺血预处理组（ｎ＝１０）;Ｅ组为缺血预处理延迟效应组（ｎ＝５）。手术后动态观察各组动物肾功能改变、组织学以及肾组织再灌注前后ＭＤＡ含量变化。结果 （１）Ｃ组术后肾功能各项指标与Ａ     

全身性非特异性免疫反应对大鼠睾丸功能的影响──Ⅱ.激素水平的变化

本实验以ＳＤ雄性大鼠为实验对象，采用碳粒血管内注射的方法，给动物造成一种全身性的非特异性免疫反应状态，以观察在这种状态下睾丸和垂体的激素分泌情况。动物经每天１次，共１０天的碳粒鼠尾静脉注射后，血浆睾酮的水平（０．８９６±０．３５８ｎｇ／ｄｌ，ｎ＝５）明显低于对照组（２．６５６±０．９９３ｎｇ／ｄｌ，ｎ＝７，Ｐ＜０．００５）；血浆ＬＨ（３．６７６±１．３５０ｍＩＵ／ｍｌ，ｎ＝９，４．６２７±２．５３９ｍＩＵ／ｍｌ，ｎ＝１０）两组比较无显著差异（Ｐ＞０．０５）；ＦＳＨ实验组（３．３６２±０．９２６ｍＩＵ／ｍｌ，ｎ＝９）与对照组相比明显降低（４．８９４±１．２３６ｍＩＵ／ｍｌ，ｎ＝１０，Ｐ＜０．０１）。实验组动物睾丸间质内ＡＣＰ阳性反应细胞增多，而β－羟基甾体脱氢酶反应消失。作者认为全身性的免疫反应既可以通过垂体也可以直接的作用于睾丸内的相关细胞，从而影响睾丸的功能。     

心跳骤停期间及心肺复苏前后前脑M受体变化的实验研究

目的 探讨心跳聚停（ＣＡ）期间及心肺复苏（ＣＰＲ）前后前脑Ｍ受体变化的规律。方法 采用窒息致大鼠ＣＡ的动物模型,５５只Ｗｉｓｔａｒ大鼠随发为正常对照组（ｎ＝８）、手术对照组（ｎ＝７）、ＣＡ１组（ｎ＝８）;窒息１０ｍｉｎ,ＣＡ２组（ｎ＝８）;窒息３０ｍｉｎ,以及ＣＰＲ前组（ｎ＝８）;窒息１０ｍｉｎ和ＣＰＲ后组（ｎ＝９）：窒息１０ｍｉｎ后复苏,自主循环恢复后继续机械通气３０ｍｉｎ,实验结束时断头取脑,     

利多卡因及山莨菪碱对大鼠急性坏死性胰腺炎病理学变化的影响

目的 探讨利多卡因及山莨菪碱对急性坏死性胰腺炎（ＡＮＰ）大鼠血淀粉酶、磷脂酶Ａ２、内毒素及其病理学变化的影响。方法 将４５只ＳＤ大鼠随机分为：①正常对照组（ＮＣ,ｎ＝１０）;②ＡＮＰ组（ｎ＝１０）;③ＡＮＰ＋生理盐水治疗组（ＡＮＰ＋ＮＳ,ｎ＝１０）;④ＡＮＰ＋利多卡因、山莨菪碱治疗组（ＡＮＰ＋ＬＡ,ｎ＝１５）。监测各组大鼠血淀粉酶、磷脂酶Ａ２、内毒素,并观察各脏器病理学改变。结果 ＡＮＰ组和ＡＮＰ     

七氟醚肝毒性研究的初步报告

为研究不同吸入浓度七氟醚对肝脏的影响，４０只ＳＤ大鼠被随机分为四组，对照组（Ｉ组，ｎ＝１０，０ＭＡＣ）；异氟醚组（Ⅱ组，ｎ＝１０，０．５ＭＡＣ）；０．５ＭＡＣ七氟醚组（Ⅲ，组，ｎ＝１０，０．５ＭＡＣ）；０．９ＭＡＣ七氟醚组（Ⅲ２组，ｎ＝１０，０．９ＭＡＣ）。各组动物分别吸相应浓度麻醉药，３ｈ／ｄ，共６ｄ，以肝功能变化，肝组织细胞这改变作为评价肝脏受损指标，结果提示，七氟醚对肝脏有一定的影响，与异氟     

七氟醚及其它挥发性麻醉药对肝药酶的影响

目的：观察七氟醚及其它挥发性麻醉药对肝药酶的影响。方法：将４０只月龄２～３月的ＳＤ大鼠随机分：对照组（Ｃ组，ｎ＝１０，０ＭＡＣ）、氟烷组（Ｆ组，ｎ＝１０，０．５ＭＡＣ）、异氟醚组（Ｉ组，ｎ＝１０，０．５ＭＡＣ）和七氟醚组（Ｓ组，ｎ＝１０，０．５ＭＡＣ）。各组动物分别吸入相应浓度的麻醉药，３小时／天，共７天。结果：表现为Ｆ组及Ｓ组肝脏代谢戊巴比妥钠的能力明显高于对照组（Ｐ＜０．０１）；Ｉ组有高于对照组的倾向（Ｐ＞０．０５）。结论：七氟醚、氟烷和异氟醚有酶诱导作用或倾向。     

脊神经节损伤介导的脊髓背角EAAs和IAAs变化的实验研究

目的：研究脊神经节（ＤＲＧ）炎性损伤时,脊髓背角兴奋性氨基酸（ＥＡＡｓ）、抑制性氨基酸（ＩＡＡｓ）含量和脊髓背角谷氨酸（Ｇｌｕ）、天门冬氨酸（Ａｓｐ）免疫组织化学的变化,及其与实验动物神经行为异常变化之间的关系。方法：健康家兔５４只,随机分为手术对照组（ｎ＝２４）;炎症损伤组（ｎ＝２４）和正常对照组（ｎ＝６）。采用组织氨基酸的含量分析仪测定脊髓背角Ｇｌｕ、Ａｓｐ、γ氨基丁酸（ＧＡＢＡ）、牛磺酸（Ｔａｕ）、苏氨酸（Ｔｈｒ）和色氨酸（Ｓｅｒ）含量,采用免疫组化法观察脊髓背角Ｇｌｕ和Ａｓｐ分布特点及变化。结果：ＤＲＧ炎症损伤介导脊髓背角ＥＡＡｓ和ＩＡＡｓ释放增加。结论：ＥＡＡｓ在痛觉过敏的形成和维持中具有重要作用,而ＩＡＡｓ的增加则与机体抗伤害性保护反应相关。ＤＲＧ炎症损伤初期,脊髓背角ＥＡＡｓ／ＩＡＡｓ动态平衡的破坏是伤害性神经细胞兴奋性损伤和伤侧肢体痛觉过敏的主要原因。     

浅低温对犬心脏停跳复苏后脑组织一氧化氮、一氧化氮合成酶和神经功能的影响

目的：一氧化氮参与机体的病理生理过程，本实验研究Ｌ－Ａｒｇ：ＮＯ通路在犬心脏停跳复苏后浅低温脑复苏中的作用。方法：１５只健康犬随机分为３组：手术对照组（Ａ组，ｎ＝４只），常规治疗组（Ｂ组，ｎ＝５只）和浅低温治疗组（Ｃ组，ｎ＝６只）。Ａ组动物只完成麻醉和手术，心脏不停跳，观察８小时；Ｂ、Ｃ两组动物完成麻醉和手术，心脏停跳１８分钟，心脏复苏成功后治疗８小时。Ｂ、Ｃ两组均给予激素和脱水治疗，Ｃ组动物在心肺复苏成功后１０分钟加用头部体表物理降温，２０分钟内将鼓膜温降至３４℃±０．５℃，维持８小时。各组动物在实验结束时行神经机能评分，开颅取右顶叶脑皮质，ＮＡＤＰＨ－ｄ组织化学显示ＮＡＤＰＨ阳性细胞、Ｇｒｉｅｓ法测定其亚硝酸盐含量。结果：（１）Ｂ组犬脑皮质ＮＡＤＰＨ阳性细胞数和亚硝酸盐含量显著高于Ａ组（Ｐ＜０．０１），Ｃ组犬脑皮质ＮＡＤＰＨ阳性细胞数和亚硝酸盐含量较Ｂ组显著降低（Ｐ＜０．０１），但ＮＡＤＰＨ阳性细胞数仍高于Ａ组（Ｐ＜０．０１）。（２）Ｃ组犬神经机能评分优于Ｂ组（Ｐ＜０．０５）。结论：浅低温具有脑复苏效应，其抑制犬心脏停跳复苏后脑组织Ｌ－Ａｒｇ：ＮＯ通路的激活，可能是其具有脑复苏效应的机理之一。     

急性坏死性胰腺炎大鼠血浆内皮素的改变及其意义

为了解急性坏死性胰腺炎（ａｃｕｔｅ ｎｅｃｒｏｔｉｚｉｎ ｐａｎｃｒｅａｔｉｔｉｓ,ＡＮＰ）时血浆内皮素（ｅｎｄｏｔｈｅｌｉｎ,ＥＴ）的变化及其病理意义,进行了前瞻性动物实验。即将ＳＤ大鼠随机分为３组：急性坏死性胰腺炎组（ＡＮＰ组,ｎ＝２）,组胆胰管注入５％牛磺胆酸钠（ＳＴＣ １ｍｌ／ｋｇ）制造ＡＮＰ模型,假手术组（ＳＯ组,ｎ＝２４）和血小板激活因子拮抗剂ＢＮ５０７３９组（ＢＮ组,ｎ＝２４）。测定     

Eeffect of seawater immersion on plasma osmotic pressure and electrolyte balance following open chest trauma

OBJECTIVE: To explore the effect of seawater immersion on serum osmotic pressure and electrolytes balance following chest trauma in dogs. METHODS: Twenty-five healthy adult dogs were used in the experiment. A canine model of right open pneumothorax was established by chest puncturing on all animals. Animals were divided into three groups: a control group (n=10) with chest trauma without any immersion; a seawater group (n=10) immersed in seawater after chest trauma and a normal saline group (n=5) immersed in normal saline solution following chest trauma. Blood samples were taken at different time intervals to determine plasma osmotic pressure and electrolytes. The hemodynamic changes were also recorded. RESULTS: Mortality in the seawater group was much higher than that of the control group and the normal saline group. The mean survival time in the seawater group lasted only 45 minutes, while in the control group and the normal saline group the average survival time was more than 4 hours (P<0.01). One of the most important causes of death was hypernatremia and high osmolality. Severe electrolytes imbalance was observed in seawater group. Hypernatremia and high osmolality were the most significant factors of high mortality in the seawater group. CONCLUSIONS: Seawater immersion after chest trauma appears to be associated with severe electrolyte imbalance as well as high osmotic pressure. These may be the risk factors leading to fatal outcome.     

胸部开放伤后海水浸泡对实验犬呼吸功能的影响

目的 探讨胸部开放伤后海水海泡所致呼吸功能障碍的病理生理特点,为研究早期救治方案提供依据。方法 实验犬致伤后随机分为对照组（n-10)和海水浸泡组（n=10)。海水浸泡组;犬于致伤后置入人工配制的海水中,于致伤前及入海水后即刻、30分钟和45分钟取动脉血测定血气分析变化,同时监测通气功能和换气功能变化。对照组：不浸泡海水,于致伤前、致伤后即刻、30分钟、45分钟、1小时、2小时、3小时和4小时进行监测,处理同海水浸泡组。结果 海水浸泡组的呼吸功能衰竭明显重于对照组,表现在严重的低氧血症和高碳酸血症,处理同海水浸泡 组。结果 海水浸泡组的呼吸功能衰竭明显重于对照组,表现在严重的低氧血症和高碳酸血症,而且出现的时间早。对照组低氧血症的主要原因是以通气／灌注比率失调为主的换气功能障碍,同时并存一定程度的限制性通气功能障碍;而造成海水浸泡组低氧血症和高碳酸血症的主要原因是以严重肺泡通气不足为主的通气功能障碍和肺内分流引起的换气功能障碍。结论 胸部开放伤后海水浸泡组与对照组所造成呼吸功能障碍的机制有所不同,前者可造成严重的Ⅱ型呼吸衰竭,对生命威胁更大。     

股骨干骨折合并脑损伤后大鼠多器官功能损害的生化指标观察

目的：对大鼠血清中多种生化指标的检测,探讨股骨干骨折合并脑损伤后对大鼠多器官功能的影响。方法：4月龄雄性SD大鼠30只,体重（280±10）g,用随机数字表法将大鼠随机分为对照组,创伤第1天组,创伤第2天组,创伤第3天组,创伤第5天组,创伤第7天组,每组5只。5个创伤组制造大鼠右侧股骨干骨折合并脑损伤的模型,然后分别在造模后第1,2,3,5,7天抽取各组腹主动脉,检测血清中天冬氨酸氨基转移酶（AST）、丙氨酸氨基转移酶（ALT）、肌酐（Cr）、尿素氮（BUN）、乳酸脱氢酶（LDH）、磷酸肌酸激酶（CK）的含量,对照组不做任何处理,只进行上述检测。对各组检测的生化指标进行比较。结果：各组血清中AST、ALT、Cr、BUN、LDH、CK含量差异均有统计学意义（P〈0．01）,其中AST、ALT、BUN、CK在创伤第1天组达到峰值（P〈0．05）;Cr在创伤第3天组达到峰值（P〈0．05）;LDH在创伤第2天组达到峰值（P〈0．05）。结论：股骨干骨折合并脑损伤后会引起大鼠血清中多种生化指标的升高,尤其以创伤后前3d的影响较为显著,这些生化指标改变可间接的反应心、肝、肾器官的功能下降。     

奥曲肽预处理对围术期肝脏缺血-再灌注损伤保护作用的临床研究

目的探讨奥曲肽预处理对围术期肝脏缺血-再灌注损伤保护作用及可能的机制。方法选择88例肝脏手术患者,随机分为研究组45例,对照组43例,术中行肝门阻断。研究组患者于手术前1h给予奥曲肽0.2mg皮下注射,对照组于手术前1h给予生理盐水1ml皮下注射。观察术前(T0)、术后6h(T1)、24h(T2)及7d(T3)时血清丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、乳酸脱氢酶(LDH),肿瘤坏死因子α(TNF-α)及白细胞介素1β(IL-1β)的变化,手术部位切除后取标本行超氧化物歧化酶(SOD)、髓过氧化物酶(MPO)的检测。采用TUNEL法检测肝组织中的凋亡细胞数。结果 T0时两组之间ALT、AST、LDH及TNF-α、IL-1β差异无统计学意义。T1时两组ALT、AST、LDH及TNF-α、IL-1β明显高于T0时(P<0.05),对照组又明显高于研究组(P<0.05)。T2时两组ALT、AST、LDH开始下降,但仍然高于T0时(P<0.05),T3时恢复正常范围,而T2、T3时TNF-α、IL-1β降至正常范围。研究组肝组织MPO明显低于对照组(P<0.05),而SOD明显高于对照组(P<0.05)。肝组织中的凋亡细胞数对照组为(67.79±5.25)明显高于研究组(44.32±5.16)(P<0.01)。结论奥曲肽对围术期肝脏缺血-再灌注损伤有保护作用,其可能的机制为稳定细胞膜、抑制炎性反应及细胞凋亡。     

New experimental model of crush injury of the hindlimbs in rats

BACKGROUND: Crush injury (CI) remains a life-threatening condition. Because there is a shortage of animal models of CI, we purposed to develop a reproducible model of CI of hindlimbs in rats and to evaluate correlation between the volume of muscles traumatized and the severity of CI. METHODS: The right or both hindlimbs of anesthetized rats were compressed for 6 hours under blocks weighing 3 kg. This was followed by 3 hours of reperfusion. Serum lactate, base excess (BE), and potassium (K) were measured at 10 minutes after cannulaton (baseline), immediately before release (compression), and 3 hours after release (reperfusion). Serum creatine phosphokinase (CK), lactate dehydrogenase (LDH), aspartate transferase (AST) and alanine transferase (ALT) were measured at baseline and reperfusion. Muscles and kidneys were evaluated morphologically. In a separate group of animals treated in the same way, survival rate was monitored for 168 hours. RESULTS: Unilateral CI did not induce serious systemic impairment. Bilateral CI resulted in severe lactic acidosis. Serum K levels increased similarly and significantly in both groups. Serum CK levels correlated strongly with the volume of muscles traumatized. Bilateral CI produced a sharp increase in serum LDH, AST and ALT levels by the end of experiment. Signs of direct cellular damage and ischemia-reperfusion injury were found in histology specimens. In bilaterally crushed rats there were patent signs of acute tubular necrosis at 24 hours after insult. All rats with unilateral CI survived, whereas mortality rate reached 58.3% in rats with bilateral CI. The majority of these animals died within 24 hours after compression. CONCLUSIONS: We developed a valid experimental model of severe CI of the hindlimbs in rats. Systemic responses to CI and the severity of CI appeared to correlate strongly with the volume of muscle traumatized.     

Synthetic sulfonolipids deduced from sulfonoquinovosyl diacylglycerols of sea urchin reduces hepatic ischemia-reperfusion injury in rats

BACKGROUND: In hepatic surgery and liver transplantation, ischemia-reperfusion (I/R) is an unavoidable process, and protection against hepatic I/R injury is a major unresolved problem. In this study, we investigated whether 3-O-(6-deoxy-6-sulfono-beta-D-glucopyranosyl)-1,2-di-O-acylglycerol bound to saturated C18 fatty acids (beta-SQAG9), which was derived from sea urchin intestines, could reduce this injury. This agent was recently reported to have immunosuppressive effects in allogeneic rat skin grafts. MATERIALS & METHODS: Male Lewis rats were divided into two experimental groups. Group 1 rats were injected with SQAG9 (50 mg/kg) into the penile vein 15 minutes before the induction of ischemia and into the portal vein just reperfusion. The same amounts of normal saline were injected into rats in the control group (group 2). Each experimental groups included six rats. Seventy percent hepatic ischemia (20 minutes) was induced by occluding the blood vessels and bile duct with a vascular clamp. For examination of hepatic function, serum levels of aspartate aminotransferase, (AST) alanine transaminase (ALT), and lactic dehydrogenase (LDH) were measured. In addition, histological examination was also assessed. RESULTS: Three hours after reperfusion, the mean plasma concentration of AST, ALT, LDH in group 1 was suppressed compared with group 2. Six hours after reperfusion, the hepatic damage in group 1 was mild in comparison with that in group 2. CONCLUSIONS: Our data demonstrated that SQAG-9 reduced the warm hepatic I/R injury.     

酮替酚和复合物48/80对肠缺血/再灌注大鼠生存率的影响

目的 观察肠缺血及再灌注后应用酮替酚和复合物48/80对大鼠生存率的影响.方法 96只健康清洁级SD大鼠(200 g～250 g)随机分为4组:S组(假手术组)、M组(缺血/再灌注组)、K组(模型+酮替酚组)及CP组(模型+复合物48/80组),每组24只.建立肠缺血75 min再灌注损伤模型.K组及CP组在再灌注前5 min及再灌注后3 d内每天分别静脉注射酮替酚1 mg/kg及复合物48/80 0.75 mg/kg,S组、M组分别给予等量生理盐水.观察各组动物第3天存活率,第3天存活大鼠肠黏膜病理及超微结构的变化,并测定血清天冬氨酸转氨酶(AST)、丙氨酸转氨酶(ALT)、AST/ALT比值(S/L)、总蛋白(TP)、白蛋白(ALB)、球蛋白(GLB)、白蛋白/球蛋白比值(A/G)、磷酸肌酸激酶(CK)、乳酸脱氢酶(LDH)、尿素氮(BUN)及肌酐(CRE).结果 与S组比较:M组存活率与TP、ALB及GLB明显降低,S/L明显升高(P<0.05),肠黏膜超微结构受损.与M组比较:K组存活率明显升高(P<0.05)和肠黏膜超微结构受损减轻;CP组存活率明显降低(P<0.05),肠黏膜超微结构受损加重.Chiu's评分各组间无统计学差异(P>0.05).CP组AST明显高于M组与K组;S/L及LDH明显高于K组(P<0.05).结论 缺血后应用酮替酚能够增加肠缺血/再灌注大鼠生存率.     

全麻复合胸段硬膜外阻滞对兔实验性心肌梗死的影响

目的 研究全麻复合胸段硬膜外阻滞（ＴＥＡ）与否对兔实验性心肌梗死的保护作用。方法 实验组兔于气管切开插管全麻复合胸段硬膜外阻滞下开胸结扎左冠状动脉前降支,在不同的时段取血,测血浆肌酸磷酸激酶（ＣＫ）、乳酶脱氢酶（ＬＤＨ）、谷草转氨酶（ＡＳＴ）活性和一氧化氮（ＮＯ）及超氧化物歧化酶（ＳＯＤ）活性的变化,对照组不作ＴＥＡ,其余处理与实验组相同。结果 实验组兔有不同时间段ＣＫ、ＬＤＨ活性变化与时间关系的     

丙泊酚对脑创伤家兔血清和脑脊液肌酸激酶、乳酸脱氢酶活性的影响

目的：观察丙泊酚麻醉对脑创伤家兔血清（s)，脑脊液（csf)肌酸激酶（CK），乳酸脱氢酶（LDH）的指标变化，探讨丙泊酚对家兔脑创伤的影响及其意义。方法：取20只健康新西兰兔建立稳定的脑创伤模型，随机分为对照组（C组）和丙泊酚组（P组），分别于伤前，伤后4，24，48，72小时和伤后7天测定血清及脑脊液CK，LDH活性。结果：C组s-CK和csf-CK,s-LDH和csf-LDH显著高于伤前（P＜0．01）,P组伤后48。72小时，7天s-CK和csf-CK显著低于C组（P＜0．01），s-LDH在伤后72小时显著低于C组（P＜0．01）,csf-LDH在伤后48小时，7天明显低于C组（P＜0．05），结论：脑创伤后，s-CK和csf-CK,s-LDH和csf-LDH活性均明显增高，丙泊酚能显著降低血及脑脊液CK、LDH活性，提示丙泊酚能够改善脑代谢，对创伤性脑损伤具有一定的脑保护作用。     

Early detection of increased tumour necrosis factor alpha (TNFalpha) and soluble TNF receptor protein plasma levels after trauma reveals associations with the clinical course

BACKGROUND: The inflammatory response after trauma includes tumour necrosis factor alpha (TNFalpha) as pro-inflammatory cytokine. Furthermore, both soluble TNF receptor proteins (sTNF-R1 and sTNF-R2) were described to influence the post-traumatic inflammatory response and organ dysfunction. METHOD: From 47 trauma patients, blood samples were obtained at the scene of accident, at hospital admission, after 4 h, 12 h, and 24 h, and daily until day 6. Plasma levels of TNFalpha, sTNFR1 and sTNF-R2 were measured by enzyme immunoassay (EIA) and analysed comparing clinical parameters such as injury scores (ISS, AIS), development of multiple organ dysfunction syndrome (MODS) and/or systemic inflammatory response syndrome (SIRS), and outcome. RESULTS: Significant changes were observed in a time-dependent manner: TNFalpha and soluble TNF receptor levels were elevated compared to values of healthy persons. At 4 h after trauma, TNFalpha and sTNF-R2 showed an increase from initial values, which continued during the entire observation period. Severe trauma led to enhanced sTNF-R1 levels on scene and on hospital admission. Development of SIRS along with elevated sTNF-R1 began on scene and was present on admission, with increased sTNF-R2 from day 1 to day 4. MODS (until day 6) was preceded by increased sTNF-R2 levels on admission and up to 4 h after trauma. Outcome was associated neither with TNFalpha nor with soluble TNF receptor levels. CONCLUSION: Thus, in trauma patients, early post-traumatic MODS and SIRS coincide with increased levels of TNFalpha and TNF receptor proteins, revealing different, time-dependent changes. Hence, detection of TNFalpha and soluble TNF receptor proteins after trauma should pay regard to the time point of sampling.