大剂量地塞米松联合乌司他丁治疗严重肺挫伤

目的：研究大剂量地塞米松联合乌司他丁治疗严重肺挫伤的疗效与安全性。方法：选择58例严重肺挫伤患者,随机分为A组（n=29）和B组（n=29）。A组接受常规治疗,包括使用地塞米松20~40mg,2次/d,连续3d。B组在常规治疗的基础上联合乌司他丁20万U加入0.9%氯化钠液100mL静脉滴注,每8h1次,连用7d;2组患者治疗第1、第7天行血气分析,并检测治疗第1、第4、第7天血清肿瘤坏死因子-α（TNF-α）、白介素-6（IL-6）的含量。比较治疗期间2组患者急性呼吸窘迫综合征（ARDS）的发生率。结果：治疗前2组血气分析指标及血清TNF-α、IL-6水平无显著差异（P〉0.05）;治疗后B组血气分析指标较同期A组显著改善（P〈0.05）,血清TNF-α、IL-6水平较A组显著下降更明显（P〈0.05）。ARDS发生率B组显著低于A组（P〈0.05）。结论：大剂量地塞米松联合应用乌司他丁能显著抑制炎症介质的释放,有效保护严重肺挫伤患者的肺功能。     

沙丁胺醇联合不同剂量布地奈德雾化吸入治疗慢性阻塞性肺疾病急性加重期的疗效观察

目的:探讨沙丁胺醇联合不同剂量布地奈德雾化吸入治疗慢性阻塞性肺疾病急性加重期(AECOPD)的临床疗效.方法:AECOPD患者121例随机分为C组(n=39)、B组(n=40)和A组(n=42),在常规治疗的基础上,C组予沙丁胺醇5 mg雾化吸入,B组、A组分别联合布地奈德1 mg、2 mg,每天雾化3次,连续治疗10 d.结果:治疗后第3 d、10 d,B组、A组呼吸困难评分和第1s用力呼气容积(FEV1)较C组明显改善(P <0.05及P <0.01),且A组较B组改善更明显(P <0.05); B、A组第10 d症状基本消失.结论:联合雾化吸入沙丁胺醇和布地奈德可明显缓解AECOPD患者呼吸困难等症状,改善肺功能,且6 mg/d较3 mg/d效果更好.     

联合应用纳洛酮与甲基强的松龙对大鼠急性肺损伤的保护作用

目的　探讨联合应用甲基强的松龙、纳洛酮对内毒素所致急性肺损伤大鼠的防治作用及可能机制。方法　建立大鼠内毒素吸入性ALI模型 (LPS ,3mg/kg气管内注射 ) ,85只大鼠随机分为生理盐水对照组、内毒素损伤组、甲基强的松龙组 (内毒素 甲基强的松龙 )、纳洛酮组 (内毒素 纳洛酮 )、联合用药组 (内毒素 甲基强的松龙 纳洛酮 )。采用放射免疫方法检测大鼠血清TNF -α、IL - 8水平 ,并观察动脉血气分析及肺组织病理变化。结果　内毒素损伤组较生理盐水组TNF -α、IL - 8水平明显增高 ,动脉血氧分压明显降低 ,肺组织可见肿胀、淤血、炎细胞浸润。联合用药组各项指标较内毒素损伤组均轻。结论　联合应用甲基强的松龙和纳洛酮可降低气管内注入内毒素致大鼠ALI血清TNF -α、IL - 8升高水平 ,减轻肺损伤病理改变程度 ,对大鼠ALI有防治作用     

补锌对重型烧伤患者细胞因子的影响

目的：探讨补锌对重型烧伤患者细胞因子水平的影响。方法：对32例重型烧伤患者随机分为治疗组（A），组服用葡萄糖酸锌口服液，口服等渗盐水为对照组（B组），于伤后当天开始用药，持续28d，检测伤后1、3、14和28d时血清内毒素，肿瘤坏死因子－α（TNF－α）和白细胞介素－6（IL－6）含量。结果：（1）在伤后1、3d,2组间血清内毒TNF－α和IL－6水平无明显差别（P＞0．05）。（2）在伤后14d及28d，A组血清内毒素、TNF－α和IL－6含量显著低于B组。结论：补锌能降低重型烧伤患者细胞因子的水平。减轻烧伤后全身炎症反应综合征（SIRS）和多器官功能障碍综合征（MODS），提高治愈率。     

充血性心力衰竭患者内皮素-1与肿瘤坏死因子-α的变化及维生素E、C的干预作用

目的 探讨充血性心力衰竭（CHF）患者肿瘤坏死因子（TNF－α）、内皮素－1（ET－1）的变化及维生素E、C的干预作用。方法 将65例心力衰竭患者随机分为两组：A组32例,给予强心、利尿、扩血管治疗;B组33例,在A组治疗药物的基础上加维生素E200mg,1次／d,维生素C 200mg,3次／d,共2周;采用特异性放免法和双抗体夹心ELTSA法分别检测65例心力衰竭患者及32例健康者血TNF－α和ET－1浓度。结果 ①充血性心力衰竭患者TNF－α和ET－1水平显著高于对照组（P＜0．01）;②两组患者治疗后心功能恢复一个级别以上,B组ET－1和TNF－α水平较A组显著下降（P＜0．05）。结论 ET－1,TNF－α参与心力衰竭的发生发展的病理生理过程,维生素E、C可降低心力衰竭患者ET－1,TNF－α水平。     

NMDA受体过度激活对严重创伤大鼠血清炎性细胞因子水平的影响

摘要：目的 观察N-甲基-D-天冬氨酸（N-methyl-D-aspartate， NMDA）受体的过度激活对大鼠严重创伤血清炎性细胞因子水平中的影响，为探索从中枢的某一环节着手，来抑制严重创伤后的炎性反应失调提供理论依据。方法 以30% TBSA Ⅲ度烧伤为严重创伤模型，利用ELISA方法检测激活NMDA受体对血清炎性细胞因子TNF-α、IL－1β、IL6水平的影响；通过膜片钳技术检测严重创伤能否导致大鼠神经元NMDA受体的过度开放；再观察阻断NMDA受体能否抑制严重烧伤后血清炎性细胞因子TNF-α、IL－1β、IL6水平的上升。结果 ①与对照组相比，使用NMDA 0.5mg/kg激活NMDA受体，血清TNF－α，IL－1β、IL6明显升高，加大剂量（2mg/kg ）可以使血清TNF－α，IL－1β、IL6进一步升高；②在35pS电导水平的开放中，烧伤使通道开放概率增加非常显著，在100pS电导水平的开放中，开放时间常数τ1、通道开放概率增加非常显著；③腹腔注射MK-801（3mg/kg）阻断NMDA受体可以抑制烧伤后血清TNF-α、IL－1β、IL6水平的上升，加大注射剂量（5mg/kg）可以进一步抑制烧伤后血清TNF-α、IL－1β、IL6水平的上升。结论 NMDA受体是严重创伤后（烧伤）大鼠血清炎性细胞因子过度升高的重要环节。     

小剂量甲基强的松龙治疗毛细支气管炎的临床观察

目的观察小剂量甲基强的松龙治疗毛细支气管炎的疗效。方法将42例毛细支气管炎患儿随机分2组。在常规治疗基础上,治疗组（n=21）应用甲基强的松龙1 mg/（kg.d）,静脉点滴,q12 h,连用5 d;对照组（n=21）采用氢化可的松5 mg/（kg.d）,1次/d,连用5 d。结果2组病例喘憋消失时间、肺部哮鸣音消失时间、住院天数比较差异有显著性（P〈0.01或P〈0.001）。小剂量甲基强的松龙治疗毛细支气管炎能迅速缓解喘憋症状,缩短疗效,明显优于氢化可的松。结论小剂量甲基强的松龙可作为毛细支气管炎患儿治疗的首选用药。     

小儿体外循环术中抑肽酶促进内源性白细胞介素-10释放的研究

目的　探讨小儿体外循环 (ECC)术中抑肽酶促进内源性IL 10释放的作用及量效关系。方法　按入选标准筛选病例并随机分成 6组 :对照组 (A1 组 ,n =15 ) ,小剂量抑肽酶组 (B1 组 ,n =15 ) ,大剂量抑肽酶组 (C1 组 ,n =15 ) ,激素组 (A2 组 ,n =2 0 ) ,激素 +小剂量抑肽酶组 (B2 组 ,n =2 0 ) ,激素 +大剂量抑肽酶组 (C2 组 ,n =2 0 )。用酶联免疫吸附试验法测定各患儿在术前 ,ECC 30min ,ECC结束后 2h ,2 4h ,7d5个时间点血清IL 10的浓度。结果　各组ECC 30min ,ECC结束后 2h血清IL 10浓度与术前相比显著增高 (P <0 0 1) ;且B1 、C1 组与A1 组相比 ,B2 、C2 组与A2 组相比及C1 组与B1 组比较 ,C2 组与B2 组比较 ,IL 10水平增高更为明显 ,各组间差异有显著性 (P <0 0 1) ;A1 、B1 组术后住院日明显延长 (P<0 0 5 )。结论　抑肽酶能促进内源性IL 10的释放 ,且药效与抑肽酶剂量呈正相关     

RRMS患者大剂量IVMP冲击治疗后激素减量方案的研究

目的:探讨复发缓解型多发性硬化(RRMS)患者大剂量静脉注射甲基强的松龙(IVMP)冲击治疗后的最佳激素减量方案。方法:选择2012年1月~2014年6月我院收治的RRMS复发期病例124例,全部患者住院后给予甲基强的松龙静脉滴注,1g/d(用500 ml生理盐水配制),连续治疗3~5 d,之后按随机数字法将患者分为四组:A组:口服泼尼松,开始60 mg/d,连续服用12d之后按10 mg/5 d的方式逐步减量;B组:口服甲泼尼龙,按48 mg/d、24 mg/d、12 mg/d各1周的方式逐步减量;C组:口服泼尼松龙,开始60 mg/d,之后按5 mg/5 d的方式逐步减量;对照组:无激素使用,无逐步减量,四组均治疗3周。结果:RRMS患者大剂量IVMP冲击治疗后,继续采用激素减量治疗的总有效率显著优于不用激素的对照组(P0.05);就不良反应发生率而言,A组不良反应发生率(16.1%)显著高于其他两种减量方案组及对照组。结果:RRMS患者大剂量IVMP冲击治疗后,采用B、C两种激素减量方案可有效缓解病情,且不良反应发生率低,推荐应用于临床治疗。     

不同剂量甲基强的松龙对哮喘急性发作的疗效观察

目的比较不同剂量甲基强的松龙对哮喘急性发作的疗效。方法25例哮喘急性发作患者采用随机方法分组，接受为期3d，1次，d的静脉滴注甲基强的松龙一次治疗。按不同给药剂量，分组如下：(1)小剂量15mg／6h；(2)中剂量60mg／6h；(3)高剂量125mg／6h。其他治疗措施如吸入性支气管扩张剂等均保持相同。测定第1秒末用力呼气量(FEV1)以定量描述对药物的反应。结果高剂量组同治疗前比较在第1天末即有显著改善，中剂量组在第2天出现改善。而低剂量组在3d内未有明显改善。高、中剂量组与低剂量组相比改善有显著差异，同时未出现严重的激素副作用。结论高、中剂量的激素具有良好的疗效，研究表明短期内使用大剂量皮质激素可显著缓解哮喘急性发作，无明显副作用，值得临床推荐使用。     

部分脾动脉栓塞后机体体液免疫的变化

目的：观察部分脾动脉栓塞治疗继发性脾功能亢进后机体体液免疫的变化。材料与方法： 32例肝炎、肝硬化、继发性脾功能亢进者,在 DSA引导下,把 5F RS型或 Yashiro导管选择性地插入脾动脉内, 1mm× 1mm× 1mm明胶海绵块 120～ 180枚与抗菌素和造影剂混合后,在透视监视下分次注入脾动脉。栓前、栓后 1、 3、 7、 14、 28和 56天分别抽血 3ml,测定血清中 IgG、 IgA、 IgE、白介素－ 2和肿瘤坏死因子的含量。结果：栓塞后动脉期,脾动脉 5级以下分支未显影,实质期 70％～ 90％脾实质未显影。栓后不同时期,血清中 IgG、 IgA、 IgE、白介素－ 2和肿瘤坏死因子含量无显著性变化。结论：部分脾动脉栓塞治疗脾功能亢进,保留了部分脾脏组织,对机体体液免疫功能无显著影响。     

脑梗死患者血清细胞因子水平与功能恢复的相关性研究

Objective To understand the pathogenetic role and clinical significance of interleukin 6(IL－ 6 ),tumor necrosis factor(TNF) and soluble interleukin－ 2 receptor(sIL－ 2R) in patients with cerebral infarction(CI) .Methods The IL－ 6,TNF and sIL－ 2R levels were measured in 46 CI patients with ELISA. Results The serum IL－ 6,TNF and sIL－ 2R levels of CI group were much higher than those of controls group .The variation of IL－ 6,TNF and sIL－ 2R levels was closely related to the size of cerebral infarction. The serum IL－ 6,TNF and sIL－ 2R levels of recovery period were much lower than those of acute period in patients with CI .Conclusions The IL－ 6 ,TNF and sIL－ 2R take part in the pathologic process after CI .The measurement of IL－ 6, TNF and sIL－ 2R is useful in determining the size of cerebral infarction.     

双异丙酚预处理对内毒素诱导的人中性粒细胞释放白细胞介素-8和肿瘤坏死因子-α及相应mRNA表达的影响

目的 探讨双异丙酚预处理对内毒素(LPS)诱导的健康成年人静脉血中性粒细胞(polymorphonuclear leukocyte,PMN)释放白细胞介素(interleukin,IL)-8和肿瘤坏死因子(tumor necrosis factor,TNF)-α的影响及其应mRNA表达的变化.方法 采集健康成人志愿者静脉血分离提纯PMN,用1640培养液制成悬液;试验分为6组:Ⅰ组(空白对照组,PMN+培养液),Ⅱ组(双异丙酚溶剂对照组,intralipid),Ⅲ组(双异丙酚组,终浓度5 mg/L双异丙酚),Ⅳ组(内毒素组,终浓度1 mg/L LPS),Ⅴ组(内毒素+溶剂对照组,intralipid+终浓度1 mg/L LPS),Ⅵ组(双异丙酚+内毒素组,终浓度5 mg/L双异丙酚+终浓度1 mg/L LPS).加药培养12h后,ELISA法检测培养上清液TNF-α、IL-8的浓度,荧光定量PCR检测PMN IL-8 mRNA、TNF-αmRNA表达量.结果 与Ⅰ组比较,Ⅳ组、Ⅴ组、Ⅵ组IL-8浓度升高,Ⅳ组TNF-α浓度升高(P<0.05);与Ⅳ组比较,Ⅵ组IL-8和TNF-α浓度降低(P<0.05).与Ⅰ组比较,Ⅳ组、Ⅴ组、Ⅵ组IL-8mRNA表达上调,Ⅳ组TNF-α mRNA表达上调(P<0.05);与Ⅳ组比较,Ⅵ组IL-8 mRNA和TNF-α mRNA表达下调(P<0.05).结论 双异丙酚预处理可通过抑制内毒素诱导的人PMN释放IL-8、TNF-α,下调JL-8、TNF-α的mRNA表达,对PMN介导的炎症反应具有抑制作用.     

脑外伤性癫痫患者炎性细胞因子和C反应蛋白变化及其临床意义

目的探讨脑外伤性癫痫患者炎性细胞因子白细胞介素-2(IL-2)、白细胞介素-6(IL-6)、肿瘤坏死因子α(TNF-α)和C反应蛋白(CRP)的变化及意义。方法选自2009年1月至2012年1月收治的脑外伤并发癫痫的患者37例,采用采用酶联免疫吸附法检测检测患者外周血中第1、3、5、7 d时IL-2、IL-6、TNF-α和CRP的水平,同时选同期20例健康人群作为对照组。结果两组1、3、5、7 d IL-2、IL-6、TNF-α和CRP水平比较差异有显著性(P<0.05,P<0.01)。脑外伤性癫痫中度、重度组IL-2、IL-6、TNF-α和CRP水平均显著高于轻度组(P<0.05)。结论脑外伤性癫痫患者外周血中IL-2、IL-6、TNF-α和CRP水平显著升高且IL-2、IL-6、TNF-α和CRP水平与病情严重程度有关,提示炎性因子与CRP对癫痫的发作有影响。     

Dynamic changes in cytokine levels in serum and synovial fluid following filtration leukocytapheresis therapy in patients with rheumatoid arthritis

We attempted to determine whether various cytokine levels in the serum and synovial fluid (SF) of rheumatoid arthritis (RA) patients are influenced by the performance of filtration leukocytapheresis (LCP). The filtration LCP procedure that used a Cellsorba® column (LCP group: n=22; responder subgroup: n=17, non‐responder subgroup: n=5) or sham apheresis (control group; n=7) was repeated three times at 1‐week intervals. Serum (LCP group, n=22; control group, n=7) and SF (LCP group, n=6; control group, n=3) samples were collected before and after LCP. Levels of tumor necrosis factor α (TNFα), interleukins (IL‐1β, IL–2, IL‐6, IL‐8, IL‐10, and IL‐15), granulocyte–macrophage colony–stimulating factor (GM‐CSF), monocyte chemoattractant protein–1 (MCP‐1), RANTES were measured by an enzyme‐linked immunosorbent assay. Serum TNFα, IL‐15, and RANTES were significantly reduced only in the LCP group. Serum IL‐10 significantly increased only in the LCP group. In the LCP subgroup, serum IL‐15, GM‐CSF, and RANTES levels were reduced significantly, while serum IL‐10 levels increased significantly only in the responder group after treatment. Serum TNFα levels were reduced significantly in both subgroups. Changes in serum IL‐10 correlated positively with the improvement of patient's assessment of pain and global severity, and physician's assessment of global severity. These results indicate that the removal of leukocytes from the peripheral blood of RA patients provokes dynamic changes in some cytokine levels in the serum and/or synovial fluid. These changes may explain some of the mechanisms by which the articular symptoms are improved by filtration LCP. J. Clin. Apheresis. 16:74–81, 2001. © 2001 Wiley‐Liss, Inc.     

Enhanced exercise-induced plasma cytokine response and oxidative stress in COPD patients depend on blood oxygenation

In healthy subjects, hypoxemia and exercise represent independent stressors promoting the exercise-induced cytokine response and oxidative stress. We hypothesized that hypoxemia in patients with chronic obstructive pulmonary disease (COPD) may affect the cytokine production and/or the changes in oxidant-antioxidant status in response to maximal exercise. Exercise-induced changes in PaO2 allowed to transiently increase or decrease baseline hypoxemia and to point out its specific action on muscle metabolism. COPD patients with severe to moderate hypoxemia (56 < PaO2 < 72 mmHg) performed an incremental cycling exercise until volitional exhaustion. Two cytokines [interleukin (IL)-6 and tumour necrosis factor (TNF)-alpha] and three blood indices of oxidative stress [plasma thiobarbituric acid reactive substances (TBARS) and two antioxidants, reduced erythrocyte glutathione (GSH), and reduced plasma ascorbic acid, RAA] were measured at rest, then during and after exercise. The changes in the cytokine levels and oxidant-antioxidant status were analysed in relation with the baseline PaO2 and its exercise-induced variations. Data were compared with those obtained in an age- and body mass index-matched group of healthy subjects. Compared with healthy subjects, COPD patients presented a marked accentuation of exercise-induced increase in IL-6 level and earlier changes in their oxidant-antioxidant status. Resting levels of IL-6 and TNF-alpha and exercise-induced peak variations of TBARS, IL-6 and TNF-alpha were negatively correlated with the baseline PaO2. In COPD patients, the peak increases in IL-6 and TBARS were attenuated when exercise hyperventilation reduced the baseline hypoxemia. Our study indicates that the PaO2 level affects both the exercise-induced oxidative stress and cytokine response in hypoxemic COPD patients.     

Targeting Oxidative Injury and Cytokines' Activity in the Treatment with Anti‐Tumor Necrosis Factor‐α Antibody for Complex Regional Pain Syndrome 1

Cytokines and oxygen free radicals have been implicated in the potential pathogenic development of complex regional pain syndrome (CRPS). We aimed to analyze the relationship between clinical status, circulating levels of cytokines, and markers of oxidative damage during the treatment with anti‐TNFα antibodies. The patient chosen for treatment had not had improvement through a number of conventional therapies and fulfilled the current diagnostic criteria for CRPS‐1. We investigated the clinical variables before and after systemic administration of 1.4 mg/kg anti‐TNFα antibody (infliximab), repeated after 1 month in a dose of 3 mg/kg. Blood samples were collected before and after anti‐TNFα antibodies administration, and plasma was analyzed for 8‐isoprostane‐prostaglandin F2α (8‐iso‐PGF2α, a marker of oxidative injury) and cytokines (TNF‐α, IL‐4, IL‐6, IL‐7, IL‐8, IL‐10, IL‐17A). Plasma concentrations of 8‐iso‐PGF2α were measured with radioimmunoassay (RIA), and the kinetics of cytokines were detected in plasma by antibody‐based proximity ligation (PLA). Pathologically high levels of 8‐iso‐PGF2α were found in the patient. Immediately after each administration of infliximab, the levels of 8‐iso‐PGF2α decreased. Although the patient showed an improvement of the cutaneous dystrophic symptoms and diminished pain associated with these lesions, the levels of circulating TNFα increased after the administration of anti‐TNFα antibodies. In a patient with CRPS‐1 treated with anti‐TNFα antibodies, we report increased levels of circulating TNFα and a temporary mitigation of oxidative stress as measured by plasma F₂‐isoprostane. This case report provides evidence 2 supporting the indication of monitoring the oxidative stress biomarkers during treatment with anti‐TNFα antibodies in CRPS 1.     

大黄对重症急性胰腺炎患者血清TNF-α、IL-1β、IL-6影响的临床研究

目的对比研究经胃管和鼻空肠管不同途径给予大黄对重症急性胰腺炎（SAP）患者血清肿瘤坏死因子α（TNF—α）、白细胞介素1β（IL-1β）和白细胞介素6（IL-6）的影响。方法SAP患者60例随机分为A组（n=20）、B组（n=20）和C组（n=20）。A组只行综合治疗,B组在综合治疗基础上给予胃管注入大黄,C组给予鼻空肠管注入大黄。观察患者入院时（0d）、7d时TNF—α、IL-1β、IL-6水平。结果入院0d时TNF—α、IL-1β、IL-6在三组中相互比较均无显著性差异（P〉0．05）。治疗7d时三组TNF—α、IL-1β、IL-6检测值均比入院时下降,其中以C组下降最明显;三组之间TNF-α、IL-1β、IL-6检测值相互比较有显著性差异（P〈0．05）。结论通过下调炎症递质的表达,鼻空肠管途径应用大黄能更有效的控制SAP的全身炎症反应。     

内毒素诱发弥散性血管内凝血伴多器官功能损害大鼠模型的建立

目的建立一种感染性弥散性血管内凝血（DIC）伴多器官功能障碍综合征（MODS）大鼠模型。方法健康清洁级Wistar大鼠24只，随机分为正常对照组、低剂量脂多糖（LPS）组、中剂量LPS组和高剂量LPS组，每组6只。正常对照组经股静脉插管两次注射不同剂量生理盐水（1．4ml／kg和2．8ml／kg）；低剂量LPS组经股静脉插管两次注射LPS1．4ml／kg（56μg／kg）和2．8ml／kg（112μg／kg）；中剂量LPS组两次注射LPS1．4ml／kg（98μg／kg）和2．8ml／kg（196μg／kg）；高剂量LPS组两次注射LPS1．4ml／kg（196μg／kg）和2．8ml／kg（392μg／kg）；两次注射间隔12h。分别经股静脉插管取各组大鼠静脉血标本，检测注射前后的血小板（PLT）、DIC凝血象、D-二聚体、纤维蛋白原（Fbg）、抗凝血酶Ⅲ（AT-Ⅲ）、血糖（Glu）、天冬氨酸转氨酶（AST）、丙氨酸转氨酶（ALT）、碱性磷酸酶（ALP）和乳酸脱氢酶（LDH）变化;第二次注射后4h，活杀大鼠取肺、肝、肾脏进行组织病理学观察。结果高剂量LPS组大鼠两次LPS攻击后4h内全部死亡；低剂量和中剂量组动物无死亡。中剂量LPS组两次LPS攻击后大鼠的PLT、D-二聚体、Fbg、Glu、AST、ALT、ALP、LDH、活化部分凝血活酶时间、凝血酶原时问和抗凝血酶Ⅲ水平与正常对照组比较差异均有显著性（P＜0．05或P＜0．01）；肺、肾、肝脏组织病理学观察均有明显的损伤改变。结论应用98μg／kg和196μg／lg LPS静脉给予对大鼠间隔12h进行两次攻击可制备DIC伴多器官功能损害大鼠模型。