全身炎症反应综合征患者胰岛素强化治疗对血清炎症介质的影响

目的研究全身炎症反应综合征患者(SIRS)施行胰岛素强化治疗对体内肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)等早期炎症介质的影响。方法68例发生应激性高血糖(血糖超过9.00mmol/L)的SIRS患者,配对后随机分为胰岛素强化治疗组和常规治疗组,分别在治疗前和治疗后第1、2和3天抽取肘静脉血3ml,采用酶联免疫吸附法(ELISA)测定血浆TNF-α与IL-6水平,并测定C-反应蛋白(CRP)变化以评估炎症程度。结果胰岛素强化治疗显著降低了SIRS患者血清TNF-αI、L-6和CRP水平,与常规治疗组比较差异有显著性,(P<0.05或P<0.01)。结论胰岛素强化治疗可拮抗SIRS患者高炎症状态,抗炎效应可能是除降血糖、促合成代谢作用之外胰岛素强化治疗又一改善SIRS患者预后的重要机制。     

IL-1、IL-6、TNF-α、CRP联合检测在维持性血液透析患者微炎症治疗中的临床应用

目的通过联合检测炎症因子白细胞介素1(IL-1)、白细胞介素6(IL-6)、α肿瘤坏死因子(TNF-α)、和C-反应蛋白(CRP),评价维持性血液透析患者治疗前后的微炎症状态。方法选择本院血液净化中心66例慢性肾衰竭患者,随机分两组,A组(对照组)不使用任何血管紧张素受体阻滞剂(ARB)、血管紧张素转换酶抑制剂(ACEI)类药物,B组(实验组)予以口服缬沙坦药物80mg/d,分别测定0月及3月后患者炎症因子IL-1、IL-6、TNF-α、CRP血清水平。结果 B组患者经过3月治疗后IL-1、IL-6、TNF-α、CRP水平降低(P<0.05),A组CRP、IL-1、IL-6水平升高(P<0.05),TNF-α水平升高不明显(P>0.05);Pearson相关性分析结果显示患者治疗后的IL-1、IL-6、TNF-α、CRP水平呈正相关。结论炎症因子IL-1、IL-6、TNF-α、CRP的联合检测可正确反映缬沙坦对维持性血液透析患者微炎症的治疗效果。     

胰岛素强化治疗对严重创伤患者炎症介质和外周血核转录因子κB的影响

目的:探讨胰岛素强化治疗对临床严重创伤患者应激性高血糖的炎症介质、外周血核转录因子κB的影响。方法:分别通过ELISA和PCR检测TNF-α、IL-6和NF-κB。结果:胰岛素强化治疗能降低血清炎症介质TNF-α、IL-6水平,能显著降低NF-κB表达。结论:胰岛素强化治疗可有效下调创伤后炎症介质水平,降低NF-κB的转录水平。     

阿托伐他汀钙联合缬沙坦对维持性血液透析患者微炎症状态的影响

目的维持性血液透析患者予以阿托伐他汀钙联合缬沙坦联合用药,观察两药联合应用与单一用药对维持性血液透析患者微炎症状态的影响。方法将56例维持性血液透析患者按随机数字表法分为A、B、C、D 4组,每组14例。A组给予阿托伐他汀钙联合缬沙坦治疗,B组给予阿托伐他汀钙治疗,C组给予缬沙坦治疗,D组未用阿托伐他汀钙和缬沙坦及同类其他药物治疗,所有患者基础治疗相同。分别在用药前及治疗12周后检测患者血清CRP、IL-1、IL-6及TNF-α水平。结果各组患者治疗前血清CRP、IL-1、IL-6、TNF-α水平比较差异均无统计学意义(P>0.05)。治疗12周后:A、B、C组血清CRP、IL-1、IL-6、TNF-α水平均较治疗前下降,其中A、C组差异有统计学意义(P<0.05),B组仅CRP差异有统计学意义(P<0.05),而IL-1、IL-6、TNF-α差异无统计学意义(P>0.05);D组血清CRP、IL-1、IL-6及TNF-α水平均较治疗前上升,其中TNF-α差异有统计学意义(P<0.05),CRP、IL-1、IL-6差异无统计学意义(P>0.05);A组与B、C组治疗后比较,炎症指标下降更明显,差异均有统计学意义(P<0.05)。结论维持性血液透析患者存在微炎症状态,阿托伐他汀钙与缬沙坦治疗均可改善维持性血液透析患者微炎症水平,且联合用药较单一用药改善作用明显。     

胰岛素强化治疗对脓毒症患者血清非特异性炎性因子表达水平及预后的影响

目的：探讨胰岛素强化治疗对脓毒症患者非特异性炎性因子表达水平及预后的影响。方法将2011年2月至2012年10月本院重症监护病房收治的50例脓毒症患者随机分为对照组和观察组,对照组患者给予常规胰岛素治疗,观察组患者给予胰岛素强化治疗,比较两组患者的预后情况及血清肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）和C反应蛋白（CRP）等血清非特异性炎性因子水平的差异。结果观察组患者 ICU入住时间短于对照组,病死率小于对照组（P＜0．05）,且两组患者治疗1、3、5、7 d后的血清 TNF-α、IL-6、CRP水平比较差异均有统计学意义（P＜0．05）。结论胰岛素强化治疗可以有效降低脓毒症患者血清 TNF-α、IL-6、CRP等炎性因子的水平,并显著改善患者的预后,值得临床推广应用。     

损伤控制外科技术对严重腹部创伤急救患者应激和炎症反应及临床结局的影响

目的:探讨损伤控制外科技术(DCS)对严重腹部创伤急救患者应激与炎症反应以及临床结局的影响。方法:选取我院2014-01-2015-12收治的55例严重腹部创伤患者作为观察组,给予患者DCS手术治疗,同时选取2012-01-2013-12收治的55例行常规确定性手术治疗的严重腹部创伤患者作为对照组,比较2组手术前后应激反应、炎症反应相关指标及临床结局。结果:观察组手术时间、术中出血量、并发症发生率均显著低于对照组(P0.05)。观察组休克、DIC、MODS发生率及病死率均显著低于对照组(P0.05)。观察组术后24h与术前相比,APS评分、APACHEⅡ总分均有明显下降(P0.01),对照组无明显变化。观察组术后24h与术前相比,血清CRP、TNF-α、IL-1β、IL-6水平均有明显下降(P0.01);对照组术后24h与术前相比,血清CRP、TNF-α、IL-1β、IL-6水平均有明显升高(P0.01);观察组术后24h血清CRP、TNF-α、IL-1β、IL-6水平均显著低于对照组术后24h(P0.01)。结论:DCS应用于严重腹部创伤患者的急救中可有效减轻机体应激反应与炎症反应,提高手术成功率。     

山莨菪碱联合乌司他丁对严重多发创伤患者血清炎症因子水平影响的研究

目的探讨山莨菪碱联合乌司他丁对严重多发创伤患者血清炎症因子肿瘤坏死因子α(TNF-α)和白细胞介素(IL)-6水平影响。方法将248例严重多发创伤患者随机分为4组,其中常规治疗组60例、山莨菪碱治疗组61例、乌司他丁治疗组62例、联合用药治疗组65例。四组患者入院均给予止血输血输液、抗感染、维持水电解质及酸碱平衡、营养支持以及呼吸循环支持等常规治疗措施;山莨菪碱治疗组在常规治疗基础上加用山莨菪碱10 mg静脉滴注,连续用药5 d;乌司他丁治疗组在常规治疗基础上加用乌司他丁20万单位+0.9%氯化钠溶液250 ml静脉滴注,1次/12 h,连续用药5 d:联合用药治疗组在常规治疗基础上加用山莨菪碱和乌司他丁静脉滴注,剂量和疗程同上两组。治疗前后采用双抗夹心法检测四组血清TNF-α和IL-6水平。结果四组治疗后血清TNF-α和IL-6水平均明显低于治疗前,且联合用药治疗组改善程度明显优于常规治疗组(P<0.01)。结论山莨菪碱联合乌司他丁对严重多发创伤患者能显著抑制炎性因子TNF-α和IL-6表达。     

IL-6、TNF-α、CRP在急性脑梗死患者血清中的表达及临床意义

目的检测白介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、C反应蛋白(CRP)在急性脑梗死患者血清中的表达并分析其临床意义。方法2015年5月至2017年8月,选取100例急性脑梗死患者、100例健康体检者,分别设为观察组、对照组。观察组依据病情轻重、病灶大小分为重、中、轻度组,大、中、小灶组。对比组间IL-6、TNF-α、CRP表达情况。结果观察组血清IL-6、TNF-α、CRP水平明显高于对照组(P<0.05)。不同病情、病灶组间的血清IL-6、TNF-α、CRP水平比较,差异有统计学意义(P<0.05)。血清IL-6、TNF-α水平:重度组>中度组>轻度组(P<0.05);血清CRP水平:重度组>中、轻度组(P<0.05)。血清IL-6、CRP水平:大灶组>中灶组>小灶组(P<0.05);血清TNF-α水平:大灶组>中、小灶组(P<0.05)。结论IL-6、TNF-α、CRP在急性脑梗死患者血清中高表达,可能参与疾病的发生发展,临床应给予重视。     

痰热清对胸科术后患者血清炎性细胞因子影响的研究

目的:探讨痰热清注射液对胸科术后患者血清炎性细胞因子水平的影响。方法:选取我院60例在全麻下行肺癌、食管癌手术患者,随机分成两组,实验组30例,对照组30例。两组均予常规预防感染等治疗,实验组在此基础上加用痰热清20mL加入5%葡萄糖注射液250mL中静脉滴注,2次/d。两组疗程均为7d。比较治疗前后两组患者血清白细胞介素-6(IL-6)、白细胞介素-8(IL-8)、肿瘤坏死因子-α(TNF-α)、C-反应蛋白(CRP)水平的变化;比较治疗后两组患者的临床治疗指标(体温、咳痰、肺部感染、白细胞)。结果:治疗7d后实验组较对照组血清IL-6、IL-8、TNF-α、CRP水平明显降低,二者比较差异有显著性(P<0.05);实验组临床疗效明显优于对照组,二者比较差异有显著性(P<0.05)。结论:痰热清注射液能降低胸科术后患者血清炎性因子TNF-α、IL-6、IL-8及CRP的水平,延缓炎症反应综合征的进程,对预防胸科术后肺部并发症具有很好的疗效。     

ω-3鱼油脂肪乳剂对严重创伤患者血白细胞介素-6及肿瘤坏死因子-α的影响

目的:探讨ω-3鱼油脂肪乳剂对严重创伤患者血白细胞介素-6(IL-6)及肿瘤坏死因子-α(TNF-α)水平的影响.方法:将29例严重创伤患者随机分为治疗组和对照组,其中,治疗组14例,对照组15例.对照组采用常规治疗,治疗组在常规治疗的基础上加用ω-3鱼油脂肪乳剂.于入院第1、3、5天收集患者血清,放入-50℃冰箱保存,统一用ELISA法检测其中促炎细胞因子IL-6及TNF-α水平,并对两组的结果进行比较.结果:入院后两组患者血IL-6及TNF-α水平均明显升高,但治疗组IL-6、TNF-α升高程度明显低于对照组(P<0.05).结论:ω-3鱼油脂肪乳剂能抑制严重创伤患者血IL-6及TNF-α水平的上升.     

How does blood glucose control with metformin influence intensive insulin protocols? Evidence for involvement of oxidative stress and inflammatory cytokines

INTRODUCTION: Recent investigations have revealed that control of hyperglycaemia with insulin improves outcomes. The cornerstone of hyperglycaemia in critically ill patients is insulin resistance and it remains refractory to intensive insulin protocols. We designed this study to evaluate the efficacy and safety of a new intensive insulin therapy (IIT) protocol combined with metformin. METHODS: Twenty-one patients with systemic inflammatory response syndrome and a blood glucose level of >120 mg/dl admitted to an intensive care unit (ICU) were randomised to receive either intravenous infusion of IIT alone (n=11) or combined with metformin (IIT+MET; n=10) to maintain a blood glucose level (BGL) of 80-120 mg/dl. Blood samples were obtained at baseline and at 48 hours, 96 hours and 7 days after initiation of the study. Samples were analysed for interleukin-6 (IL-6), tumour necrosis factor alpha (TNF-alpha) and nitric oxide (NO) as inflammatory mediators; plasminogen activation inhibitor-1 (PAI-1) as a coagulation mediator; and thiobarbituric reactive substances (TBARS), total antioxidant power (TAP) and total thiol molecules (TTM) as oxidative stress parameters. RESULTS: The addition of metformin to the IIT protocol decreased insulin requirement and concentration of insulin and C-peptide. With both treatments at most time points, the mean plasma levels of IL-6, TNF-alpha, NO, PAI-1 and TBARS were found to be significantly lower compared with baseline. Antioxidant activity was increased in both arms with increasing TAP and TTM (P<0.05). There was no significant difference between the two groups regarding reported beneficial effects on these parameters. Therapeutic Intervention Scoring System-28 (TISS-28) score, an index of nursing workload and number of therapeutic interventions, decreased in the IIT+MET group (P<0.01). We did not observe any occurrence of hyperlactataemia or acidosis in the IIT+MET group. CONCLUSION: Metformin plus insulin appears to lower the incidence of insulin resistance, lower insulin requirement while maintaining blood glucose level control, and consequently lower the incidence of adverse effects related to high-dose insulin therapy, particularly hypoglycaemia, and also declined nursing workload. Both treatment protocols showed improvements in inflammatory cytokine levels. Further studies with larger sample sizes are warranted to determine the undiscovered facts of insulin-sensitising agents in critically ill patients.     

胰岛素强化治疗对创伤患者免疫球蛋白、补体及单核细胞噬菌能力的影响

目的探讨胰岛素强化治疗对严重创伤患者血清免疫球蛋白与补体水平的变化以及外周血单核细胞大肠杆菌颗粒吞噬能力的影响。方法采用随机配对原则将外科重症加强治疗病房（ICU）收治的创伤严重度评分（ISS）〉20分的严重创伤患者分为胰岛素强化治疗组（目标血糖值4～6mmol／L）和常规治疗组（目标血糖值〈11．1mmol／L）。分别在入院时及入院后2、4、6和8d留取外周静脉血，检测血清免疫球蛋白（IgA、IgG、IgM）与补体（C3、C4）水平的动态变化，全血细胞与用异硫氰酸荧光素（FITC）标记的大肠杆菌共孵育后检测单核细胞噬菌能力。结果两组严重创伤患者血清IgA、IgG、IgM和C3、C4水平在入院时均较低，入院治疗后均开始升高，并在治疗6～8d达到或接近正常范围。胰岛素强化治疗后C3、C4水平明显低于常规治疗组（P均〈0．05），并呈现恢复延迟的特点，而血清IgA、IgG、IgM水平两组比较差异均无显著性（P均〉0．05）。强化治疗组患者治疗4d和6d单核细胞大肠杆菌吞噬能力比入院时显著增强，且2、4和6d的大肠杆菌FITC阳性率均显著高于常规治疗组（P均〈0．05）。结论胰岛素强化治疗能明显改善严重创伤后免疫功能，增强单核细胞噬菌能力，是提高患者机体抵抗力的有效方法之一。     

Increased levels of tumour necrosis factor-alpha (TNF-alpha) in patients with Type II diabetes mellitus after myocardial infarction are related to endothelial dysfunction

The pathophysiology of insulin resistance and atherosclerosis may share a common inflammatory basis, maintaining endothelial dysfunction, suggesting why patients with T2DM (Type II diabetes mellitus) have an impaired prognosis after an MI (myocardial infarction), but it remains unclear how these parameters are inter-related. Forty patients with an MI (20 patients with and 20 patients without T2DM) took part in this cross-sectional study. Endothelium-dependent [FMD (flow-mediated dilation)] and -independent [NTG (nitroglycerine)] vasodilatation (determined by ultrasound), S(I) (insulin sensitivity index; determined by isoglycaemic-hyperinsulinaemic clamp) and serum levels of CRP (C-reactive protein), TNF-alpha (tumour necrosis factor-alpha), IL-6 (interleukin 6), resistin and adiponectin (determined by ELISA) were measured. Associations between FMD/NTG and S(I), and CRP, TNF-alpha, IL-6, adiponectin, resistin, lipids, blood pressure, BMI (body mass index) and brachial artery diameter were then assessed. FMD (2.1 compared with 4.7%; P<0.05), NTG (14.9 compared with 21.2%; P<0.05) and S(I) [4.3 compared with 6.6 10(-4) dl.kg(-1) of body weight.min(-1).(mu-units/ml)(-1); P<0.05], and adiponectin levels (3.1 compared with 6.4 microg/ml; P<0.01) were all lower in patients with T2DM. TNF-alpha (6.9 compared with 1.8 pg/ml; P<0.01) and IL-6 (2.3 compared with 1.2 pg/ml; P<0.01) levels were higher in patients with T2DM, whereas differences in CRP and resistin levels did not attain statistical significance between the two groups. TNF-alpha concentrations and brachial artery diameter were negatively, whereas S(I) was positively, correlated with FMD. Adjustment for age weakened the association for S(I), whereas TNF-alpha and brachial artery diameter remained significantly associated with FMD after adjustment for group, age and BMI. Endothelial dysfunction and low-grade inflammation co-exist in T2DM after MI. These results suggest that the endothelium is negatively impacted in multiple ways by the diabetic state after an MI.     

Arteriovenous carboxyhemoglobin difference is not correlated to TNF-alpha, IL-6, PCT, CRP and leukocytes in critically ill patients

BACKGROUND: It is still unclear as to whether the paradoxical arteriovenous carboxyhemoglobin (COHb) difference found in critical illness may represent a novel marker of the acute inflammatory response. We determined whether the arterial and central venous COHb concentration or their difference may be correlated to classical pro-inflammatory markers. METHODS: Arterial and matched central venous blood gases were obtained from non-smoking intensive care patients undergoing gastrointestinal surgery, and were correlated with plasma concentrations of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), procalcitonin (PCT), C-reactive protein (CRP) and leukocytes. RESULTS: No correlation was found between arteriovenous COHb difference and the investigated pro-inflammatory mediators. While arterial and central venous COHb concentrations were positively correlated to plasma concentrations of TNF-alpha (P< or =0.01), IL-6 (P<0.05) and PCT (P< or =0.01), they were neither interrelated with PCT nor with leukocytes. CONCLUSIONS: Arteriovenous COHb difference does not appear to be a marker of the acute inflammatory response. Future studies are needed to investigate whether arterial and central venous COHb concentrations by themselves may serve as indicators of systemic inflammation.     

血浆置换对重型病毒性肝炎患者血清细胞因子的影响

目的 :观察重型病毒性肝炎患者血清细胞因子的变化 ,探讨血浆置换疗法对患者的影响。方法 :随机选择 4 0例经血浆置换治疗的重型病毒性肝炎患者 ,测定治疗前后血清肿瘤坏死因子 α(TNFα)和白介素 4(IL 4 )的水平 ,观察其与预后、肝功能、并发症间的关系。结果 :4 0例患者经治疗后 TNFα由 (79.32±2 2 .39) ng/L 下降到 (2 0 .0 1± 2 2 .2 5 ) ng/L(P<0 .0 0 1) ,IL 4由 (0 .6 1± 0 .0 7) ng/L 降至 (0 .5 7± 0 .0 6 ) ng/L(P<0 .0 1) ,好转出院的患者较恶化出院的患者下降尤其明显 (P均 <0 .0 5 ) ;肝功能的恢复同样是好转出院的患者较恶化出院的恢复得更好 (P <0 .0 5或 P <0 .0 1) ;对嗜睡、定向能力均有明显改善 (P<0 .0 1和 P <0 .0 5 ) ,对治疗各种并发症更好 (P<0 .0 1)。结论 :血浆置换能清除 TNFα和 IL 4 ,是防治各种并发症的有效措施。预后不佳者与炎症的持续存在导致血清中 TNFα和 IL 4水平较高有关。     

Altered plasma cytokines and total glutathione levels in parenterally fed critically ill trauma patients with adjuvant recombinant human growth hormone (rhGH) therapy

OBJECTIVES: Glutathione (GSH) is a potent endogenous antioxidant that serves as one of the body's most important defenses against oxygen metabolites. Plasma levels of GSH are maintained primarily by a balance between secretion from the liver and degradation in the kidney. The ability to maintain and enhance tissue GSH may be of particular importance in controlling cytokine production in response to a stimulus like injury. The interaction after severe trauma between GSH and cytokines, tumor necrosis factor (TNF) -alpha, and interleukin (IL)-6, are not known. The purpose of the study was to investigate the levels of plasma GSH and cytokines TNF-alpha and IL-6 in adult patients admitted to the intensive care unit of our level I trauma center who were treated with recombinant human growth hormone (rhGH) for > or =7 days. DESIGN: Prospective, randomized, controlled trial. SETTING: Trauma intensive care unit. PATIENTS: Twenty-eight patients with multiple injuries and 14 normal postabsorptive controls. INTERVENTIONS: From 48-60 hrs after injury, when resuscitation was complete, a stable hemodynamic status was achieved and the patients were receiving maintenance fluid without nitrogen or calories, a blood sample was drawn for basal, plasma GSH, TNF-alpha, and IL-6 measurement. Intravenous feeding was then started and continued for 7 days. The patients were randomized to receive or not to receive daily intramuscular doses of recombinant human growth hormone (0.15 mg rhGH/kg/day). Daily morning plasma was obtained for analysis of GSH, TNF-alpha, and IL-6 levels. RESULTS: In the early catabolic "flow phase" of severe injury, the plasma levels of GSH were not altered but plasma TNF-alpha and IL-6 levels were increased significantly, compared with uninjured controls. Seven days of total parenteral nutrition alone enhanced plasma GSH levels (76%), but no change in TNF-alpha was observed. Supplementation with rhGH enhanced GSH (180%), and TNF (65%) with no changes in IL-6 levels. There is a significant linear relationship between plasma GSH and TNF-alpha levels in our rhGH-supplemented trauma patients. CONCLUSION: Modification of plasma GSH and TNF-alpha levels by adequate nutritional support with adjuvant rhGH during the postinjury period demonstrates the beneficial role of GSH in enhancing antioxidant defenses.     

Circulating cytokines as markers of systemic inflammatory response in severe community-acquired pneumonia

OBJECTIVES: To assess the influence of empirical antibacterial therapy on systemic inflammatory response in patients with severe community-acquired pneumonia (CAP). MATERIAL AND METHODS: Thirty consecutive patients with CAP meeting systemic inflammatory response syndrome (SIRS) criteria were recruited into this study. Blood samples for measurement of interleukin-6 (IL-6), interleukin-8 (IL-8), interleukin-10 (IL-10) and C-reactive protein (CRP) concentrations were drawn on days 1, 3, 5, 7 and 10. For analysis, these patients were divided into two subgroups according to British Thoracic Society (BTS) severity score and to clinical response to the initial antibacterial therapy. RESULTS: In the group with severe CAP (n= 15), serum concentrations of IL-6 (P = 0.0001), IL-8, (P = 0.001), IL-10 (P = 0.0001) and CRP (P = 0.0001) were significantly higher compared to patients from the non-severe group (n= 15). IL-6 presented with a sharp decrease between days 1 and 3 in non-responders with severe CAP (P = 0.004). IL-6 concentrations on day 1 were significantly associated with a response to empirical antibacterial treatment by day 3. CONCLUSION: Despite the absence of a clinical response to empirical antibacterial treatment as assessed by conventional clinical parameters on day 3 in patients with severe CAP meeting SIRS criteria, there was a marked reduction in the degree of the systemic inflammatory response as reflected by IL-6 levels.     

Effects of polyenylphosphatidylcholine on cytokines,nitrite/nitrate levels,antioxidant activity and lipid peroxidation in rats with sepsis

OBJECTIVES: To determine the effect of pretreatment with polyenylphosphatidylcholine (lecithin, PPC) on plasma levels of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, IL-10, total nitrite/nitrate (NOx), and tissue levels of superoxide dismutase (SOD) and malondialdehyde (MDA) in septic rats. DESIGN: Prospective, randomized, controlled animal study. SETTING: University laboratory. SUBJECTS: Forty-five Spraque-Dawley rats were divided into three groups: group C, sham-operated; group S, sepsis; and group P, sepsis pretreated with PPC. INTERVENTIONS: Rats were made septic by cecal ligation and puncture (CLP). Group P rats were treated with PPC (100 mg/day orally) for 10 days before sepsis. Twenty-four hours later CLP, plasma concentrations of TNF-alpha, IL-6 and IL-10 and plasma levels of NOx were measured. SOD and MDA were determined in liver, lung and heart homogenates. MEASUREMENTS AND MAIN RESULTS: All rats in group P survived during the 24-h observation time after CLP, whereas survival rate in group S was 66.7% (10/15; P<0.05). PPC significantly reduced plasma levels of TNF-alpha (P=0.006), IL-6 (P=0.007), IL-10 (P=0.016), NOx (P<0.001), and tissue levels of MDA (P<0.001) in group P with respect to in group S. Tissue levels of SOD significantly increased in group P when compared with group S (P<0.001). CONCLUSIONS: These results show that PPC pretreatment exerts cumulative effects in decreasing the levels of cytokines, NOx, and tissue MDA concentrations, with a concomitant increase in survival in septic rats. Lecithin therapy may be a useful adjuvant therapy in controlling of the excessive production of the inflammatory cytokines in patients with severe sepsis. DESCRIPTOR: SIRS/sepsis, experimental studies.