巯基化合物对内毒素诱导大鼠枯否细胞NF—kB活性和肿瘤坏死因子释放的影响

目的 观察巯基化合物对内毒素诱导大鼠枯否细胞（KC）NF-kB活性和肿瘤坏死因子-a（TNF-a）释放的影响。方法采用胶原酶灌注和percoll密度梯度离心法分离得到高纯度大鼠KC，在过夜培养后冲洗两遍（不含血清），加入内毒素（LPS）10ng／ml刺激原代培养的KC，观察不同浓度谷胱甘肽乙基酯（GSHEE）及N-乙酰半胱氨酸（NAC）对大鼠KCTNF-a释放和KC内谷胱甘肽（GSH）及NF-kB活性的影响。并观察使用谷胱甘肽合成抑制剂BSO后，对NAC抑制炎症因子的影响，采用凝胶滞留电泳法测NF-kB活性，采用高效液相色谱分析法测GSH水平。结果 LPS诱导KC中GSH水平无变化；GSHEE和NAC可提高KC中GSH水平（P〈0．05），降低NF-kB活性和TNF-a释放（P〈0．05）。NAC与BSO合用时KC中GSH水平无变化，TNF-a释放降低（P〈0．05）。结论 NAC通过抑制KC中NF-kB的激活和TNF-a的释放调节KC功能，但这种抑制作用并非通过增加GSH介导。     

白藜芦醇甙对内毒素刺激小鼠腹腔巨噬细胞产生TNFα和NAG的影响

收集小鼠腹腔巨噬细胞，调整细胞浓度为５×１０￣５／ｍｌ，加入２４孔培养板每孔１ｍｌ，内毒素刺激前后不同时间加入白藜芦醇甙培养，检测上清中肿瘤坏死因子，溶酶体酶（Ｎ－乙酰－β－Ｄ氨基葡萄糖苷酶ＮＡＧ）的变化，结果说明：白藜芦醇甙可减少上清中ＴＮＦ＿α和ＮＡＧ的量，通过此可减少内毒素刺激产生的由ＴＮＦ＿α和ＮＡＧ介导的组织损伤。     

内毒素导致白细胞急剧升、降10倍一例报导

目的探索白细胞(WBC)数小时内急剧升、降原因。方法收集患者入院时首次血、尿细菌培养结果;取患者1周内7次EDTA-K2抗凝血标本,在STKS全自动血细胞分析仪上,与高、中、低定值全血质控品同时进行比对测定,每个样本平行分析4次求均值,同时检测患者6次血清标本内毒素含量,统计数据。结果测得仪器批内误差CV0.18%;其中14小时内5个样本WBC均数(x)分别为20.1×109/L、2.3×109/L、3.2×109/L、22.8×109/L、15.7×109/L;血、尿均分离到大肠埃希氏菌,内毒素试验阳性。结论内毒素导致WBC贴壁,造成病危期4小时内周围血液WBC急剧下降10倍;临床在分析实验结果时既要考虑内毒素导致WBC上升,又要考虑内毒素致使WBC贴壁造成急剧下降现象。     

地塞米松对内毒素休克新生大鼠脑一氧化氮合成酶基因表达的调节

目的：探讨新生大鼠内毒素休克脑损伤时脑一氧化氮合成酶(NO6)三种亚型基因表达的变化及地塞米松(DEX)对其的调控作用。方法：在新生大鼠内毒素休克动物模型基础上，采用逆转录PCR及PCR技术，对脑组织中三型NOS mRNA及caspase—3 mRNA的表达进行半定量分析。结果：正常新生大鼠脑iNOS及eNOS mRNA无明显表达，nNOS mRNA、caspase—3 mRNA有一定程度表达。内毒素脂多糖(LPS)腹腔注射后2h，三种亚型NOS mRNA开始表达，于LPS6h达高峰，并持续至24h。caspase—3 mRNA于LPS腹腔注射后2h后表达逐渐增加，24h达高峰。DEX可抑制nNOS、iNOS及caspase—3 mRNA的表达，且以用药后2h最为明显，并持续至用药后24h。结论：内毒素休克脑损伤时，各型NOS均有表达，NO的产生是内毒素休克脑损伤时重要的病理生理机制之一。DEX通过抑制NOS、caspase—3 mRNA的表达部分实现其神经保护作用．     

连续肾替代治疗对严重烧伤脓毒症患者血浆内毒素和细胞因子水平的影响

目的　分析连续肾替代治疗 (continuousrenalreplacementtherapy,CRRT)对严重烧伤脓毒症患者血浆内毒素和细胞因子水平的影响。　方法　对 10例应用CRRT及 10例应用常规疗法治疗的严重烧伤脓毒症患者血浆内毒素和细胞因子 (TNFα、IL 1β、IL 6、IL 8)浓度变化进行比较分析。　结果　严重烧伤脓毒症患者应用CRRT后血浆内毒素、细胞因子浓度较治疗前明显下降 ,其下降速度与常规治疗组比较差异有非常显著性意义 (P <0 .0 1)。　结论　严重烧伤脓毒症患者应用CRRT能有效降低血浆内毒素和细胞因子浓度     

Management of abdominal sepsis

Introduction: Today the management of the different forms of peritonitis is generally standardised. The classification of primary and secondary peritonitis is well accepted. From a pathophysiological point of view, postoperative and post-traumatic peritonitis should be considered as independent entities. The bacteriological isolates from the inflamed peritoneal cavity do not correlate with the clinical course, and the occurrence of enterococci and bacteroides may be slightly related to ongoing infectious complications. Classification: Valuable scoring systems mainly rely on systemic signs of the septic disease and seem to better differentiate the prognosis of the disease than more surgically oriented scores do. Although the scoring systems did not allow any clinical decision, they should be used to help better compare patients treated in different institutions. The observation of the minor relevance of bacteriology and the superiority of general sepsis scores agrees with the fact that pre-existing septic organ dysfunction and pre-existing comorbidity are the main determinants of mortality. Treatment: Surgical therapy focuses on the control of the source of infection because it has been clearly shown that, without resolving the source of infection, the prognosis remains poor. Adjuvant surgical measures aim at the further reduction of the bacterial load in the peritoneal cavity. Planned relaparotomy, relaparotomy on demand, and continuous closed peritoneal lavage are used. Results: Clinical results proved these methods to be equally effective although pathophysiological considerations favour closed peritoneal lavage. Conclusion: Summarising the available data, we need a more sophisticated understanding of the pathophysiology of the peritonitis, and well-designed clinical studies are necessary to define the optimal surgical treatment modalities. Received: 27 November 1997     

肾上腺素对内毒素致大鼠炎症性肝损害的保护作用

目的 探讨肾上腺素（Epi）对内毒素（脂多糖，LPS）致大鼠炎症性肝损害的保护作用及其作用机制。方法 50只SD大鼠随机分为5组（每组各10只）：对照组：静脉滴注生理盐水2．4mL·kg^-1·h^-1；LPS组：静脉注射LPS6mg·kg^-1后，静脉滴注生理盐水2．4mL·kg^-1·h^-1；低、中和高剂量Epi组：静脉注射LPS6mg·kg^-1后，分别静脉滴注Epi0．12、0．3和0．6μg·kg^-1·min^-1。在LPS注射前、注射后2和6h3个时点取血，检测血清ALT、AST、TNF-α、IL-1β和IL-10水平，并在6h时点观察肝脏的组织病理学改变。结果 LPS组注射LPS后2、6h血清AST和ALT水平较对照组显著升高。同时血清TNF-α、IL-1β和IL-10水平亦较对照组显著升高（P〈0．05）。病理检查结果示：LPS组肝窦扩张、充血，局灶性肝细胞坏死。高剂量Epi可显著降低血清AST和ALT水平，减轻肝脏病理损伤，并显著可降低TNF-α水平和升高IL-10水平（1）8LPS组，P均〈0．05），但对IL-1β水平无影响。中、低剂量Epi对LPS致炎症性肝损害无明显保护作用。结论 Epi可通过抗炎作用减轻LPS诱导的炎症性肝损害。     

Response of body temperature and serum iron concentration to repeated pyrogen injection in rabbits

We measured body temperature and serum iron concentration after five daily consecutive injections of febrile doses of Salmonella typhosa lipopolysaccharide (0.1 g/kg) and two doses of Staphylococcus aureus cell walls (1×10⁷ and 5×10⁷ cells) in rabbits. Tolerance to endotoxin injection, as manifest by a significant attenuation in the body temperature elevation, developed after the first injection of endotoxin. The endotoxin-induced fall in serum iron concentration was attenuated significantly by the 5th day of endotoxin injection. In contrast, no tolerance developed in either the body temperature or serum iron response following repeated daily injections of S. aureus. Rabbits rendered tolerant to endotoxin showed normal febrile and serum iron responses to subsequent S. aureus injection. Rabbits given serial injections of S. aureus, although not tolerant to S. aureus itself, exhibited attenuated body temperature responses but not serum iron responses to endotoxin injection. We suggest that repeated injection of endotoxin diminishes the ability of endotoxin to stimulate endogenous pyrogen (EP) synthesis and/or release, a property not shared by the gram-positive pyrogen S. aureus. However, repeated injection of S. aureus weakens the central endotoxin-EP pathway.     

Regulation of cytokine synthesis in cardiac surgery: Role of extracorporeal circuit and humoral mediators <Emphasis Type="Italic">in vivo</Emphasis> and <Emphasis Type="Italic">in vitro</Emphasis>

Objective and design: Cardiopulmonary bypass (CPB) impairs monocyte and neutrophil proliferation, cytokine synthesis, and antigen presentation. This study compares in vivo data with results from an extracorporeal circulation (ECC) model, distinguishing direct effects on cytokine synthesis from regulatory mechanisms. Patients and methods: Whole blood from 18 patients prior to, during and after CPB was stimulated with lipopolysaccharide (LPS). Tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-8 levels were measured. Additionally, blood from 4 volunteers was circulated in an ECC model. Cytokine levels were measured before and during mock ECC. Results: LPS-induced cytokine synthesis was reduced after CPB (TNF-α: 11 %; IL-6: 29 %; IL-8: 48 % of preoperative values, all p < 0.001). In mock ECC, cytokine production (except IL-8) was suppressed: TNF-α production was lowest 60 min after starting ECC, IL-6 synthesis was lowest at 90 min (33 % and 15 % vs. pre-ECC levels; both p < 0.001). Patient sera contained cytokine-inhibitory activity after CPB, an activity not found in mock ECC. Conclusions: (1) In patients, CPB induces early transient LPS hyporesponsiveness; (2) blood contact with foreign surfaces induces LPS hyporesponsiveness; (3) serum cytokineinhibitory activities are released after CPB, but not in mock ECC. Impaired leukocyte function may explain increased susceptibility to infections after CPB. Received 16 September 2006; accepted without revision by K. Visvanathan 18 October 2006     

精氨酸加压素对家兔血细胞生成内生致热原的影响

本文观察了精氨酸加压素对体外培育的兔全血细胞产生内生致热原的影响。结果表明，ＡＶＲ对内毒素诱生ＥＰ过程有明显抑制作用；而ＡＶＰ单独与血细胞培养无降温物质产生；同时，所用剂量的ＡＶＰ对ＥＰ性发热无直接抑制作用。因此作者认为，ＡＶＰ１能够抑制ＥＴ诱生家兔血细胞生成ＥＰ，这可能是其降低或阻断ＥＴ性发热的主要机制之一。