EFFECTS OF ACUPUNCTURE ON THE CONTENTS OF ENKEPHALINS IN DIFFERENT BRAIN REGIONS AND CORTICOSTERONE IN PLASMA OF RATS WITH ENDOTOXIN SHOCK

In this experiment,we have observed the effects of acupuncture on the contents ofenkephalins in different brain regions and corticosterone in plasma of rats with endotoxin shock.Theresults showed that after acupuncture the endogenous enkephalins were significantly decreased(P【0.05)in the midbrain and brain stem of endotoxin shock rats,suggesting the anti-shock of acupuncture might be related to the enkephalins in the midbrain and brain stem.In addition,there was a rising trend in plasma corticosterone of the rats with toxic shock.

Comparison between the protective effects of removing circulatory TNF by specific immunoadsorption and by nonspecific Amberlite XAD-7 adsorption on experimental endotoxin shock

Objective: To compare the protective effects of removingcirculatory TNF by specific immunoadsorption and by nonspeciflc Amberlite XAD-7 adsorption on experimental endotoxin shock. Methods: New Zealand white rabbits receiving a lethal dose of endotoxin underwent hemoperfusion through immunoadsorbent or Amberlite BAD-7. Plasma TNF levels. efficiency of the adsorbents and the survival rate were observed. Results: After 2 h of hemopcrfusion through immunoadsorhent or Amberlite XAD-7. plasma TNF levels were significantly lower than those in the control group(P<0.01). and the best result was shown by immunoadsorption (P<0. 01). The 12 h and 18 h survival rates were 70% and 30% in the immunoadsorption group, and 30% and 5% in the Amberlite XAD-7 group respectively (P<0. 05). Conclusion: Compared with the nonspecific Amberlite XAD-7 adsorption,the specific imrnunoadsorption might be a more effective method of removing circulatory TNF and improve the survival rate in endotoxin shock.

Study on Modified Shengmai Yin Injection for Prevention and Treatment of Brain Impairment in Endotoxin Shock Rats

Objective:To examine the effects of modified Shenmai Yin on invigorating vital energy, promoting blood flow, and protection against neural impairment in an endotoxin-induced shock rat model. Methods: Ninety-six SD rats were randomly divided into four groups: sham operation (saline 20 ml/kg), shock model (lipopolysaccharide, LPS, 8 mg/kg), Reformed Shengmai Yin (加味生脉饮 Pulse-activating Decoction) (LPS 8 mg/kg + reformed Shengmai Yin Injection 10 ml/kg), and dexamethasone (LPS 8 mg/kg + dexamethasone 5 mg/kg) groups. Each group was subdivided into 1 h, 2 h, 3 h, and 6 h time points for observation. The carotid artery was separated and connected with a biological functional system to monitor mean arterial pressure (MAP). Brain water levels, malonaldehyde (MDA) content, and superoxide dismutase (SOD) activity were also determined. Results: In the shock model group, MAP was progressively decreased after injection of LPS, brain water and MDA contents were increased, brain SOD activity was decreased, and capillary vessel edema in brain tissue was also observed. All these parameters were improved significantly in both treatment groups, although the effects were more marked with Shengmai Yin than with dexamethasone. Conclusion: Modified Shengmai Yin exhibits strong anti-shock and neuroprotective effects against Endotoxininduced shock.

ROLE OF ENDOGENOUS CARBON MONOXIDE IN ENDOTOXIN SHOCK

Objective.To study the role of endogenous carbon monoxide (CO) in endotoxin shock. Methods. The changes of CO levels and the effects of zinc protoporphyrin IX (ZnPP),an inhibitor of hemeoxygenase (HO), in endotoxin shock and the efficacy of hemin,an inducer of HO were investigated. Results.The plasma CO levels were found to be significantly increased during the course of endotoxin shock. Injection of ZnPP was shown to abrogate the endotoxininduced hypotension and metabolic derangements markedly. Administration of hemin to healthy rabbits revealed the hypotension and metabolic derangements similar to the animals given endotoxin. Conclusion.CO is a newly found endogenously produced mediator which may play an important role in the pathogenesis of endotoxin shock.

oXiris-内毒素吸附技术治疗ESRD合并脓毒症患者的临床效果观察

目的探讨oXiris-内毒素吸附技术治疗终末期肾病(end-stage renal disease,ESRD)合并脓毒症的疗效。方法回顾性收集2020年1月1日—2023年7月30日于河南科技大学第一附属医院住院治疗的ESRD合并脓毒症患者41例,其中oXiris组22例,连续性静脉-静脉血液滤过(continuous veno-venous hemofiltration,CVVH)联合血液灌流(hemoperfusion,HP)组19例。比较2组患者住院死亡率、ICU住院时长、机械通气时长、连续性肾脏替代治疗时长、机械通气患者数、使用滤器数以及在血液净化治疗开始时及治疗后急性生理与慢性健康评分(acute physiology and chronic health evaluation,APACHE-Ⅱ)、去甲肾上腺素(norepinephrine,NE)用量以及实验室检查结果。结果oXiris组患者机械通气时长少于CVVH+HP组(Z=-3.749,P=0.001)。治疗后oXiris组APACHE-Ⅱ评分(t=-4.481,P=0.001)、NE用量(t=-2.036,P=0.049)、C反应蛋白(Z=-2.850,P=0.004)、白细胞介素-6(Z=-2.512,P=0.012)水平较CVVH+HP组降低。结论oXiris-内毒素吸附技术能有效降低ESRD合并脓毒症患者炎症介质,且效果优于CVVH+HP,具有良好的临床应用价值。

血清ADMA、IL-6、内毒素及乳酸在新生儿败血症所致感染性休克中的表达及临床意义

目的探讨血清不对称二甲基精氨酸(ADMA)、白细胞介素-6(IL-6)、内毒素及乳酸在新生儿败血症所致感染性休克中的表达及临床意义。方法选取我院收治的58例新生儿败血症所致感染性休克患儿为休克组,62例新生儿败血症未发生感染性休克患儿为败血症组,60例无感染新生儿为对照组。检测所有研究对象血清中的ADMA、IL-6、内毒素及乳酸水平。比较三组研究对象的ADMA、IL-6、内毒素及乳酸水平;分析ADMA、IL-6、内毒素及乳酸水平对新生儿败血症所致感染性休克患儿的诊断价值;分析ADMA水平与IL-6、内毒素及乳酸水平的关系;分析ADMA、IL-6、内毒素及乳酸水平与休克组预后的关系。结果休克组的ADMA、IL-6、内毒素及乳酸水平均高于败血症组及对照组(P<0.05);败血症组的ADMA、IL-6、内毒素水平均高于对照组(P<0.05);败血症组和对照组的乳酸水平无显著差异(P>0.05)。受试者工作特征曲线(ROC)结果显示,ADMA、IL-6、内毒素及乳酸诊断新生儿败血症所致感染性休克的曲线下面积(AUC)分别为0.93、0.89、0.89、0.92。Pearson相关性分析结果显示,ADMA水平与IL-6、内毒素及乳酸水平呈正相关(P<0.05)。ADMA、IL-6、内毒素及乳酸高水平与新生儿败血症所致感染性休克预后不良有关。结论血清ADMA、IL-6、内毒素及乳酸在新生儿败血症所致感染性休克中表达水平较高,可作为该疾病诊断的生物标志物并预测预后。

Effect of cholecystokinin octapeptide on mean pulmonary artery pressure in endotoxic shock rats

Objective:To investigate the effects of CCK-8 on mean pulmonary artery pressure in rats with endotoxic shock.Methods:Male SD rats were randomized into seven groups(n=6):control group,model group,LPS+CCK-8 group,CCK-8 group,CCK-1R antagonist group,CCK-2R antagonist group,DFSO+PF group.The rats were induced to lethal endotoxic shock by an injection of LPS(30 mg.kg-1).CCK-8(50μg.kg-1)was administered 30 min after LPS injection.Either a specific CCK-1R antagonist or CCK-2R antagonist was injected before CCK-8 treatment.The mean arterial pressure(MAP)and mean pulmonary artery pressure(MPAP)were collected by a multi-channel data physiological recorder.As well as the 8h mortality was recorded.Results:Compared with control group,the MAP were significantly continuously lower and the MPAP significantly higher in model group.Administration of CCK-8 significantly delayed the LPS-induced not only decreases in MAP but also rises in MPAP,while reduceing the mortality.In addition,the specific antagonist at the CCK-2 receptor(CCK-2R)abrogated the action of CCK-8 significantly.Conclusion:while the LPS-induced hypotension delayed,CCK-8 could effectively alleviate the LPS-induced rises in MPAP via the CCK-2 receptor in ES rat model,while reduceing the mortality.

Changes of Lipid Peroxides and Superoxide Dismutase in Visceral Tissues during Endotoxic Shock in Rats

As compared with the control,the malondialdehyde(MDA)levels in the cardi-ac,pulmonary,and intestinal tissues were elevated(P【0.05),and the superoxide dismu-tase activities in the cardiac,pulmonary,and intestinal tissues increased(P【0.05)at the30th min after endotoxic shock;the former in the cardiac,hepatic,renal,pulmonary,andintestinal tissues were elevated(P【0.05～0.001)and the latter in the cardiac,pulmona-ry,and intestinal tissues decreased in the 2nd h after shock;and the former were marke-dly elevated(P【0.01～0.001)and the latter severely decreased(P【【0.05～0.001)in allthe visceral tissues tested in the 4th h after shock.These data showed that lipid peroxid-ation mediated through oxygen-derived free radicals brought about tissue damage of theviscera listed above,which occurred earlier in the heart,the lungs and the intestines thanin the liver and the kidneys,and superoxide dismutase(SOD)activity was suppressed inthe late stage of endotoxic shock.

血清乳酸、降钙素原、内毒素对脓毒症及感染性休克预后的预测价值

目的探究乳酸(Lac)、降钙素原(PCT)、内毒素(ETX)在血清中的水平对脓毒症及感染性休克预后的预测价值。方法选取郑州市第一人民医院2019年2月至2022年2月收治的脓毒症患者和感染性休克患者103例作为研究对象,根据病情程度分为单纯脓毒症组(65例)、感染性休克组(38例)。对比两组血清Lac、PCT、ETX水平,Spearman相关性系数分析各血清指标与脓毒症和感染性休克病情程度的相关性。随访28 d,判定两组预后情况,对比不同预后患者血清Lac、PCT、ETX水平,受试者工作特征(ROC)曲线分析三者单独及联合预测预后的价值。结果感染性休克组血清Lac、PCT、ETX水平高于单纯脓毒症组,差异有统计学意义(t=13.815、5.740、5.945,P<0.05);血清Lac、PCT、ETX与脓毒症病情程度呈正相关(r=0.784、0.626、0.701,P<0.05);单纯脓毒症组、感染性休克组死亡者血清Lac、PCT、ETX水平高于生存者(t=3.876、3.806、4.056、3.413、3.001/4.188,P<0.05);血清Lac、PCT、ETX联合预测单纯脓毒症预后、感染性休克预后的AUC值分别为0.878、0.858,均大于各指标单独检测0.802、0.810、0.748、0.813、0.794、0.714(P<0.05)。结论脓毒症患者存在血Lac、PCT、ETX高表达情况,且与病情程度、预后关系密切,联合检测可为临床评价病情程度及预后提供客观依据,指导制定治疗方案。

Protective effects of bactericidal/permeability-increasing protein against hemorrhagic shock and its mechanism

Effects of bactericidal/permeability-increa protein(BPI, 1. 5 and 3. 5 rug/kg iv at the beginning of shock and resuscitation respectively) on the outcome of hemorrhagic shock was investigated in rats. Itwas found that BPI administration could improve hepatic and renal functions after hemorrhagic shock, andenhance the survival rate of the rats with shock (BPI group: 81 % vs physiological saline group: 44 %, P <0.05). In BPI group, the plasma endotoxin level was not significantly changed (0. 20± 0. 04 at the end of resuscitation vs 0. 24± 0. 05 U/ml before shock). Tumor necrosis factor. and interleukin-6 levels in BPI group, although higher after shock and resuscitation, were significantly lower than those in physiologia saline group.It is suggested that BPI exerts a protective effects on rats with hernorrhagic shock, which might be due to itsaction against hemorrhage-induced endotoxin translocation and its inhibition of cytokine responses in shock,

淋巴液对内毒素休克大鼠的干预作用及其机制

目的 观察外源性正常淋巴液对脂多糖 (LPS)所致大鼠内毒素休克的干预作用 ,初步探讨其作用机制。方法 Wistar雄性大鼠 4 0只 ,随机分为内毒素组、淋巴液组、血浆组、正常组。前 3组复制内毒素休克模型 (LPS ,5mg/kg·bw ,iv) ,正常组以等量生理盐水代替LPS。 15min后 ,淋巴液组输入仅占全血量 1/ 15的无细胞淋巴液。血浆组以血浆代替淋巴液 ,内毒素组和正常组以生理盐水代替淋巴液。给予LPS后 4h,取血浆及心、肝、肾、肺组织匀浆 ,对比观察血浆及组织中肿瘤坏死因子 -α(TNF -α)、一氧化氮 (NO)、一氧化氮合酶 (NOS)、诱导型一氧化氮合酶 (iNOS)、超氧化物歧化酶 (SOD)及丙二醛 (MDA)含量的变化。结果 淋巴液干预后 ,淋巴液组血浆TNF -α水平为 18.81± 3.70fmol/mL、NO含量为 4 6 .0 2± 9.2 9μmol/L、NOS活性为 2 5 .16± 4 .2 0U/mL、SOD活性为 10 2 .15± 17.88NU/mL、MDA水平 8.19± 1.6 4nmol/mL ,与其余 3组相比 ,各项指标差异均有统计学意义 (P <0 .0 5～ 0 .0 1)。结论 外源性正常淋巴液对内毒素休克具有干预作用 ,其机制可能与减少细胞因子及自由基损伤有关。

大黄对大鼠肠粘膜及肠血管通透性的影响

目的：研究大黄对肠粘膜及肠血管通透性的影响。方法：选用低血容量性休克和内毒素性休克大鼠动物模型，以荧光标记白蛋白和小肠湿／干重比值检测内毒素性休克肠血管通透性，以血浆内毒素含量来衡量肠粘膜通透性。结果：内毒素能引起小肠组织明显水肿，其湿／干重比值显著增高，同时明显提高肠血管壁对荧光标记白蛋白的通透性；而大黄能减轻肠壁水肿和湿／干重比值（内毒素组为３．７５±０．６８，大黄组为１．６６±０．３３，Ｐ＜０．０１），降低肠血管通透性〔小肠组织荧光标记白蛋白含量：内毒素组为（１．２５４±０．１１７）μｍｏｌ／ｇ，大黄组为（０．９００±０．０７１）μｍｏｌ／ｇ，Ｐ＜０．０１〕。低血容量性休克能破坏肠粘膜屏障，提高肠粘膜对内毒素的通透性，而大黄可明显降低低血容量性休克大鼠肠粘膜通透性，抑制肠道内毒素的吸收〔血浆内毒素含量：休克组为（０．５５７±０．０６９）ＥＵ／ｍｌ，大黄组为（０．３４５±０．０５５）ＥＵ／ｍｌ，Ｐ＜０．０１〕。结论：大黄能保护肠粘膜屏障，抑制肠道内毒素吸收，降低肠粘膜及肠毛细血管通透性。

大黄对胃肠动力学影响的基础和临床研究

目的：研究大黄对胃肠动力学的影响。方法：对动物模型（内毒素性休克大鼠）和临床病例进行了监测。结果：内毒素明显抑制肠道跨膜电位〔正常对照组（５９．６３±０．６５）ｍＶ，内毒素休克组（５５．５１±１．５３）ｍＶ〕有显著性差异；大黄可提高内毒素性休克大鼠肠道跨膜电位（５９．３４±０．８７）ｍＶ。临床３６例应激性胃肠粘膜病变伴出血患者经大黄治疗后，３０例显效（其中１８例止血效果良好），６例发生再出血；８例应用Ｈ２受体阻滞剂止血，２例显效，后均发生再出血；１２例采用Ｈ２受体阻滞剂配合冰盐水加去甲肾上腺素（ＮＥ）止血，５例显效，以后均发生再出血。４９例中毒性肠麻痹患者经大黄治疗后，４１例恢复肠蠕动，其中２４例能耐受２０９０ｋＪ／ｄ以上的要素饮食；而２７例应用Ｈ２受体阻滞剂的患者，无一例恢复肠蠕动。结论：大黄能提高胃肠道平滑肌的兴奋性，促进胃肠蠕动，对应激性胃肠粘膜病变亦有较好的疗效。

人参二醇组皂甙对内毒素性休克保护作用机制的实验研究

将粗制大肠杆菌内毒素注入大鼠腹腔复制休克模型。用128只Wistar大鼠随机分成内毒素休克组(ESG),内毒素休克·人参二醇组皂甙预治疗组(ESPG),对照组(CG)。结果发现:ESPG组大鼠16h存活率高于ESG组(P<0.05),肺组织过氧化脂质含量则低于ESG组,两组差异显著(P<0.005);ESPG组大鼠8h、16h血清过氧化脂质含量低于ESG组(P<0.05),两组差异显著(P<0.05);血清和肺ESPG组去甲肾上腺素、5-HT含量低于ESG组。提示人参二醇组皂甙具有明显的抗休克作用。

白藜芦醇甙对大鼠内毒素休克的影响

用经煮沸灭活及反复冻融的大肠杆菌O_(111)B_4混悬液8×10^(10)/ml,静注复制大鼠内毒素休克模型,观察比较给白藜芦醇甙予先处理后再形成的内毒素休克大鼠与休克对照组。结果表明:白藜芦醇甙改善了内毒素休克大鼠的血压下降和血中白细胞,血小板的减少;各时点脉压差的降低明显大于休克对照组,表明心血管功能的代偿能力有所改善。对用白藜芦醇甙后如白细胞和血小板的改变,血浆中溶酶体和肿瘤坏死因子的释放减少和血细胞比积不升高进行了讨论。

大黄对肠粘膜屏障的保护作用

本研究旨在证明大黄是否对出血性休克大鼠肠粘膜屏障具有保护作用。实验用雄性ＳＤ大鼠，右侧颈动脉放血，血压５．３２ｋＰａ（４０ｍｍＨｇ）维持１ｈ，失血回输，观察２４ｈ。大黄（１５０ｍｇ／ｋｇ）于复苏后即刻、６ｈ、１２ｈ分次经胃管注入。实验结果：①内脏含菌量：大黄治疗组大鼠各器官含菌量明显低于休克组和安慰剂治疗组（Ｐ＜０．０１）。②血浆内毒素水平：复苏后２４ｈ，大黄治疗组大鼠血浆内毒素水平明显低于休克组和安慰剂治疗组（Ｐ＜０．０１）。③病理形态学改变：大黄治疗组小肠病理改变程度明显轻于休克组和安慰剂治疗组。提示：大黄对出血性休克大鼠肠粘膜屏障有明显保护作用。

人参二醇皂苷对失血性休克复合内毒素二次打击大鼠肺组织水通道蛋白1表达的影响

目的:观察失血性休克复合内毒素(LPS)二次打击大鼠肺泡毛细血管内皮细胞膜水通道蛋白1(AQP1)的表达变化及人参二醇皂苷(PDS)和糖皮质激素(Dex)对其影响。方法:通过失血性休克复合LPS二次打击建立稳定的急性肺损伤模型,分为假手术对照组(S)、二次打击模型组(HL)、Dex预治疗组(HLD)及PDS预治疗组(HLP);应用HE染色观察肺组织病理学变化,采用RT-PCR、Western blotting及免疫组织化学检测AQP1的表达。结果:①病理组织学结果显示,HL组肺组织可见较弥漫的间质炎性改变,肺泡间隔明显增宽,肺间质内有大量的炎性细胞浸润,可见灶性出血,肺泡腔变小,部分腔内含有水肿液;而HLD组及HLP组大鼠肺脏改变明显减轻。②HL组肺组织AQP1 mRNA及蛋白表达水平均低于其他各组(P<0.05);免疫组织化学检测,肺泡周围毛细血管内皮细胞AQP1呈弱阳性,而HLD组及HLP组AQP1 mRNA及蛋白表达量明显高于HL组(P<0.05)。结论:失血-LPS二次打击可使大鼠肺组织中AQP1的表达减少,加重肺损伤,是肺水肿形成的原因之一;Dex与PDS能使其表达提高,从而起到减轻肺水肿的作用;PDS与Dex有减轻失血性休克复合内毒素二次打击诱导的肺损伤作用。

活血化瘀中药对内毒素性休克内皮细胞的保护作用

目的 :探讨活血化瘀中药对内毒素性休克大鼠肺微血管内皮细胞的保护作用。方法 :选 Wistar大鼠 ,随机平分为对照组、模型组 (L PS)、地塞米松治疗组 (Dex)和活血化瘀中药治疗组 (AMRS)。电镜观察内皮细胞的超微结构改变 ,用电脑图像分析系统进行形态计测及肺微血管通透性指数 (PMPI)和循环内皮细胞 (CEC)数量的测定。结果 :AMRS组与 L PS组比较内皮细胞厚度极明显减小 (P<0 .0 0 1) ,胞饮泡体密度、细胞表面破损线密度、PMPI及 CEC数量均有明显差异 (P<0 .0 1或 P<0 .0 5 )。 AMRS组与 Dex组比 ,上述大多数指标有显著差异 (P均 <0 .0 5 ) ,微血管内血小板聚集、纤维素沉着和白细胞粘附内皮细胞现象也明显减少。结论 :在内毒素性休克中 ,活血化瘀中药在超微结构水平上能够改善、修复受损的内皮细胞 。

活血化瘀药对内毒素休克大鼠细胞因子释放的影响

目的 :探讨活血化瘀药对内毒素休克大鼠细胞因子释放的影响。方法 :Wistar大鼠 40只 ,随机平分为对照组 (NS)、内毒素休克组 (L PS)、地塞米松治疗组 (Dex)和活血化瘀药治疗组 (AMRS) 4组 ,分别检测各组血中内皮素 1(ET 1)、一氧化氮 (NO)、肿瘤坏死因子α(TNFα)和超氧化物歧化酶 (SOD)的浓度变化。结果 :在 L PS刺激下 ,血中 ET 1、NO和 TNFα的浓度与 NS组比较显著增加 (P均 <0 .0 1) ,而 SOD较 NS组浓度降低 (P<0 .0 5 )。 Dex组与 L PS组比有不同程度的恢复 ,但只有 ET 1降低明显 (P<0 .0 5 )。 AMRS组的各项指标均与 L PS组比有显著差异 (P均 <0 .0 5 )。结论 :AMRS影响 L PS刺激所诱导的血中 ET 1、NO、TNFα和 SOD浓度的改变 ,其在内毒素休克过程中对内皮细胞等靶细胞释放细胞因子具有重要的调节作用。

用cDNA微阵列研究内毒素休克小鼠肺组织基因表达谱的改变

利用cDNA微阵列检测了小鼠内毒素休克 2h及 2 0h肺组织基因表达谱的改变 .发现内毒素休克 2h有12 8个基因表达上调 ,3个基因下调 ;内毒素休克 2 0h有 5 1个基因表达上调 ,2 1个下调 .并用RT PCR进一步验证了结果的可靠性 .初步分析了基因表达谱改变的意义 .