肝硬化大鼠出血性休克后血内毒素,TNF—α,NO水平的变化及其与？…

此研究观察了经大鼠出血性休克后血内毒素、ＴＮＦ－α、ＮＯ水平的变化及其与门静脉压力的关系,结果表明：出血性休克可以在门静脉高压大鼠引起明显的内毒素血症,以及继发性血浆肿瘤坏死因子和一氧化氮水平的升高;小剂量多粘菌素Ｂ的事先使用可以抑制这种反应。内毒素移位知肝硬化伴门静脉高压大鼠出血性休克后的高水平门静脉压的维持中起重要作用。     

脾切除及大肠杆菌内毒素攻击对大鼠血浆内毒素,TNF和NO水平…

本实验动态观察了大鼠脾切除及粗制大肠杆菌内毒素攻击后血浆内毒素、肿瘤坏死因子（ＴＮＦ）和ＮＯ２＾－／ＮＯ３＾－水平的变化。结果发现：脾切除组较假手术组血浆上述因子均明显升高（Ｐ〈０．０５或Ｐ〈０．０１），且和单纯腹腔注射大肠杆菌内毒素后所引起的改变非常类似。注射内毒素后，切脾前后血浆上述因子无明显差异，但均处在较高水平上，秩相关分析表明：血浆ＮＯ２＾－／ＮＯ３＾－与内毒素及ＮＴＦ水平有一定相关性（     

脾切除及大肠杆菌内毒素攻击对大鼠血浆内毒素、TNF和NO水平的影响

本实验动态观察了大鼠脾切除及粗制大肠杆菌内毒素攻击后血浆内毒素、肿瘤坏死因子（ＴＮＦ）和ＮＯ－２／ＮＯ－３水平的变化。结果发现：脾切除组较假手术组血浆上述因子均明显升高（Ｐ＜０．０５或Ｐ＜０．０１），且和单纯腹腔注射大肠杆菌内毒素后所引起的改变非常类似。注射内毒素后，切脾前后血浆上述因子无明显差异，但均处在较高水平上，秩相关分析表明：血浆ＮＯ－２／ＮＯ－３与内毒素及ＴＮＦ水平有一定相关性（ｒｓ分别为０４２２及０７２１，Ｐ均＜００１），其中与ＴＮＦ高度相关。作者认为：脾切除后机体免疫力下降，可能导致肠道细菌或毒素移位，诱导产生ＴＮＦ等细胞因子，并协同激活体内Ｌａｒｇ：ＮＯ通路。这也可能是脾切除后凶险性感染（ＯＰＳＩ）发生机制之一。     

门静脉高压症大鼠内毒素血症与一氧化氮变化

本研究拟通过测定门脉高压大鼠血浆内毒素和亚硝酸根/硝酸根离子(NO_2~-/NO_3~-)浓度,探讨一氧化氮(NO)在鼠门高压时产生是否过多及其可能机制.雌性SD大鼠分为三组:端侧门腔分流(PCS,n=10),门静脉部分缩窄引起的肝前型门高压(PHT,n=10)和手术对照组(Sham,n=8).模型制备后两周测定门脉压(FPP)并从腹主动脉采集血样,用于测定(1)血浆亚硝酸根/硝酸根离子浓度;(2)血浆内毒素浓度;(3)肝、肾功能.结果显示:血浆内毒素和NO_2~-/NO_3~-水平是PCS>PHT>Sham,且血浆内毒素与NO_2~-/NO_3~-之间呈密切正相关,提示门脉高压时因门体分流和肝功能减退导致血浆内毒素水平升高,刺激NO合成与释放增多.     

肝硬化自发性腹膜炎患者血浆、腹水内毒素和TNF-α检测及其意义

目的 研究肝硬化腹水患者血浆、腹水中内毒素（LPS）和肿瘤坏死因子（TNF-α）水平及其与自发性细菌性腹膜炎（SBP）、肝功能分级之间的关联。方法 采用鲎试剂三肽显色基质偶氮法及酶联免疫吸附法（ELISA）检测60例正常人的血浆、62例肝硬化腹水患者血浆、腹水LPS和TNF-α水平，并测定血清谷丙转氨酶（ALT）、总胆红素（TBIL）、凝血酶原时间（PT）。结果 无论有无合并SBP，肝硬化患者的血浆LPS、TNF-α及脚、TBIL、PT水平均明显高于对照组，而合并有SBP组高于无SBP组（P〈0．05）。结论 检测血浆及腹水中的LPS和TNF-α水平有助于早期诊断SBP，对临床病情严重程度分级、指导治疗以及判断疗效有一定辅助作用。     

家兔创伤休克后血浆内毒素,TNF和IL—6的动态变化

目的：探讨创伤休克对内毒素移位的影响及其与ＴＮＦ、ＩＬ－６产生的关系。方法：选用家兔１６只，随机分为创伤合并失血性休克（Ⅰ组）和单纯失血性休克组（Ⅱ组），采用鲎试验基质显色法，ＥＬＩＳＡ和细胞生物测定法分别测定血浆内毒素、ＴＮＦ和ＩＬ－６水平。结果：休克１．５小时，Ⅰ组血浆内毒素水平即明显高于伤前，至复苏后０．５小时达峰值，复苏后１小时仍明显高于伤前。休克后Ⅰ组血浆内毒素水平明显高于Ⅱ组；休克及复苏后，血浆ＴＮＦ、ＩＬ－６水平也先后显著升高，其中ＴＮＦ升高较早，Ⅰ组血浆细胞因子水平明显高于Ⅱ组；相关分析表明，创伤休克后血浆ＴＮＦ、ＩＬ－６均值分别与血浆内毒素均值呈显著正相关。结论：创伤休克可导致明显的内毒素血症及ＴＮＦ、ＩＬ－６等细胞因子过量产生，且较单纯休克时明显，创伤后细胞因子产生与内毒素移位有一定的内在联系。     

TNFα、NO在烧伤复合内毒素血症早期肾损害中的作用及其意义

目的 探讨肿瘤坏死因子α(TNFα)、一氧化氮(NO)在烧伤合并内毒素血症早期肾脏损害中的作用及其意义。方法 以大鼠体表烧伤Ⅲ度20％TBSA合并小剂量内毒素(1mg／kg体重)腹腔注射造成多脏器损害模型,按设计分组并在致伤后不同时相点进行肾脏病理形态学观察、TNFα和NO血清浓度测定、TNFα mRNA原位杂交和iNOS免疫组化染色。结果 烧伤后注射内毒素组诱导型一氧化氮合酶(iNOS)的表达和NO的合成以及TNFα mRNA的表达和TNFα的血浆水平均显高于和早于单纯烧伤组和单纯注射内毒素组。结论 烧伤合并内毒素血症时肾组织中NO和TNFα的水平显升高,两的升高可能是导致肾脏损害和引起肾脏血流动力学改变的重要因素之一。     

免疫吸附清除循环肿瘤坏死因子对内毒素休克的保护作用

观察免疫吸附清除循环肿瘤坏死因子对内毒素休克的治疗作用。方法利用新西兰白兔内毒素休克模型，研究经抗ＴＮＦ单克隆抗体亲和免疫吸附柱血液灌流对血压、肝、肾功能及成活率的影响。结果免疫吸附治疗后血浆ＴＮＦ水平迅速降低，动物血压及肝、肾功能显著改善，早期成活率明显提高。结论应用免疫吸附疗法清除循环ＴＮＦ可能是一条治疗内毒素休克的有效途径     

失血性大鼠休克后肠、肝、肺组织中细胞因子表达、释放时相及其伴随的病理变化

目的：探讨休克后促炎细胞因子的表达、释放时相及伴随的肠、肝、肺组织病理变化。方法：80只SD大鼠随机均分为失血性休克组和对照组。采用RT-PCR、ELISA方法检测失血性休克后30、60、90min及复苏后30、90min肠、肝、肺组织内TNF-α、IL-6 mRNA表达及血清中TNF-α、IL-6含量；HE和IHC染色检测伴随的组织病理变化。结果：①休克30min时，肠、肝、肺内的促炎细胞因子表达未见升高；60min时肠道先出现TNF-αmRNA表达升高（P〈0．05）：而肝脏在90min开始表达升高（P〈0．05），肺脏则在复苏后30min开始表达升高（P〈0．05）。复苏后90min肠、肝、肺的细胞因子表达都继续显著升高（P〈0．01）。②TNF-α 在肠、肝、肺的表达升高最早，其后为IL-6 mRNA。③30min时门静脉和外周血中TNF-α、IM的含量与对照组相比无显著差异，而60min时门静脉血中含量显著升高（P〈0．01）。④休克后肠黏膜坏死脱落；肝组织结构紊乱、肝窦增宽、肝细胞变性坏死；肺脏间质水肿、炎症细胞浸润。结论：失血性休克时细胞因子的释放顺序是肠道、肝脏和肺脏，推测存在“肠-肝-肺”细胞因子释放轴的可能，有待进一步确定。     

血清NO、NOS和TNF-α与外科感染的关系

目的:探讨血清NO、NOS和TNF-a与外科感染的关系.方法:30例外科感染病人血清标本,分别用化学法和酶联免疫反应法测定NO、NOS、TNF-a含量.结果:外科感染病人血清NO、NOS、TNF-a含量均高于正常对照组(P＜0.05),治疗后病人血清NO、NOS、TNF-a含量较治疗前变化明显(P＜0.05).结论:NO、NOS、TNF-a在外科感染时升高,好转则下降.     

肝硬变门脉高压休克再灌注胃粘膜损伤的实验研究

本实验应用电子自旋共振（ＥＳＲ）技术及自旋捕捉剂ＰＢＮ直接测定肝硬变门脉高压（ＰＨＴ）大鼠胃粘膜在休克再灌注前后及应用超氧化物歧化酶（ＳＯＤ）、丹参（ＲＳＭ）治疗后氧自由基（ＯＦＲ）的动态变化，同时检测胃粘膜中ＳＯＤ活性，并观察同期胃粘膜的光镜、电镜病理改变。结果：ＰＨＴ胃粘膜在休克再灌注过程中有大量ＯＦＲ产生，粘膜损伤的严重程度与ＯＦＲ含量及ＳＯＤ活性密切相关；ＰＨＴ胃粘膜更易受休克再灌注时ＯＦＲ的损伤，早期应用抗氧化剂ＳＯＤ及ＲＳＭ，可通过不同机理减轻胃粘膜再灌注损伤。     

人胆囊组织内巨噬细胞、肿瘤坏死因子、IL-1的含量变化与胆结石的关系

收集人体胆囊６３份，其中１６份无结石为非结石组，４７份为有胆固醇结石之胆囊为结石组。测定胆囊组织巨噬细胞（Ｍ）数量、胆囊粘膜肿瘤坏死因子（ＴＮＦ）、白细胞介素－１（ＩＬ－１）的含量。结果：结石组胆囊组织内Ｍ数量明显高于非结石组（分别为４１０１．９０±２９５．７２、５７２．１３±３０．０７ＡＵ，Ｐ＜０．０１）；结石组胆囊粘膜ＴＮＦ、ＩＬ－１的含量亦显著高于非结石组（ＴＮＦ分别为１８．１２±２．０３、４．４５±０．３９ｎｇ／ｍｇ，Ｐ＜０．００１。ＩＬ－１分别为１０２．４２±７．８４、６６．７５±９．５０ｕ／ｍｇ蛋白，Ｐ＜０．０５）。结果提示：胆囊组织Ｍ中的活化及其释放的ＴＮＦ、ＩＬ－１与胆囊组织炎症反应和胆囊结石的形成有内在联系。     

射频治疗原发性肝癌前后可溶性白细胞介素-2受体和肿瘤坏死因子的变化

目的　研究原发性肝癌患者集束电极射频治疗前后血清可溶性白细胞介素 - 2受体 (SIL - 2 R)和肿瘤坏死因子(TNF)水平的变化及其临床意义。方法　采用 EL ISA双抗体夹心法 ,检测 4 2例原发性肝癌 (HCC)患者集束电极射频治疗前后血清 SIL - 2 R和 TNF的表达水平的改变 ,并与健康对照组比较 ;分析 SIL - 2 R和 TNF与 AFP的相关性。结果　治疗前 HCC患者血清 SIL - 2 R和 TNF水平明显高于对照组 (P<0 .0 1) ;集束电极射频治疗后 1周 ,血清 SIL - 2 R和 TNF水平无明显变化(P>0 .0 5 ) ;治疗后 2周 ,血清 SIL - 2 R和 TNF水平降低 ,与治疗前比较差异有显著性 (P<0 .0 1) ,但仍高于对照组 (P<0 .0 1) ;血清 SIL - 2 R/ TNF水平与 AFP水平不相关。结论　原发性肝癌患者集束电极射频治疗后血清中 SIL - 2 R和 TNF水平下降 ,机体免疫功能增强 ;并可作为早期诊断、病情判断、复发检测的重要指标     

THE IMPACT OF CHRONIC RENAL FAILURE ON NITRIC OXIDE SYNTHASE ISOFORMS GENE EXPRESSION IN THE PENIS AND PELVIC GANGLIA OF RATS

PURPOSE: Patients with chronic renal failure experience a variety of physical and metabolic alterations. Uremia is often accompanied by erectile dysfunction (ED). Little information is available concerning the underlying pathophysiological mechanisms by which chronic renal failure can lead to erectile dysfunction. In this study, chronic renal failure was induced by 5/6 nephrectomy in a rat model. Cavernous nerve stimulation was used to measure the intracavernous pressure (ICP) rise. MATERIALS AND METHODS: Adult male Sprague-Dawley rats, aged between 10-12 weeks and weighing 200-250 gm. were divided into two groups. The first group (n = 20) served as a control (sham-operated) and underwent laparotomy with dissection of the perirenal fat around both kidneys. The second group (n = 40) were subjected to an excisional 5/6 nephrectomy (unilateral nephrectomy and contralateral upper and lower polar nephrectomy). Serum creatinine was measured 3 days post-operatively and at the end of the 12th week. Development of renal failure was considered if the animal had serum creatinine more than 120 microM/l. After 12 weeks, 10 animals per group were subjected to electric field stimulation (EFS) of the cavernous nerve with simultaneous recording of ICP-rise and systemic blood pressure. Northern and western blot analyses were used to determine the mRNA expression and protein contents of NOS isoforms (neuronal and endothelial) in the penile tissues and MPG. RESULTS: This remnant kidney model resulted in renal failure in 20 of 40 animals. The ICP-rise after cavernous nerve stimulation in the renal failure group was significantly impaired, 7.7+/-2.9 cm. H2O, as compared to control rats, 55.5+/-1.2 cm. H2O (p<0.001). The latency period after cavernous nerve stimulation was significantly increased in renal failure rats (6.9+/-0.95 sec.) in comparison to controls (2.4+/-0.25 sec.). Six of ten uremic animals had significantly lower testosterone (<1 nmol./l.) levels compared to non-uremic rats (3.6 nmol./l.) (p<0.005). Northern blot analysis revealed that renal failure rats had significantly higher levels of nNOS mRNA in the MPG and penile tissues than controls. There was no change in eNOS mRNA in either group. Western blot analysis demonstrated that eNOS and nNOS protein contents in the MPG and penile tissues of renal failure rats were significantly higher than those of controls. CONCLUSION: This report demonstrates that impairment of erection in renal failure rats, as determined by ICP-rise, was present in spite of elevated neuronal nitric oxide synthase mRNA and its protein in the MPG and penile tissues. Further studies are needed to determine whether erectile dysfunction is a result of post-translational changes, circulating inhibitory substances or other factors.     

一氧化氮,血栓素／前列环素及ATP与肝硬变大鼠肝脏缺血再灌注损伤

四氯化碳复制大鼠肝硬变模型，通过大鼠肝脏缺血再灌注损伤模型，比较硬变肝与正常肝在缺血再灌注损伤时的差异和意义。结果显示：肝硬变时对缺血再灌注损伤反应与正常大鼠不同，再灌注时肝脏一氧化氮合成释放显著增加，肝组织ＡＴＰ含量明显降低且长时间难以恢复等，可能是肝硬变时对缺血再灌注损伤更敏感、更易发生肝功能衰竭的重要原因。     

EFFECT OF ACUTE HYPOCAPNIA ON RENAL FUNCTION IN THE DOG ARTIFICIALLY VENTILATED WITH NITROUS OXIDE, OXYGEN AND HALOTHANE

Changes from normocapnia to hypocapnia (and vice versa) wereinduced in dogs lightly anaesthetized with nitrous oxide andhalothane and subjected to passive pulmonary ventilation. Duringhypocapnia estimated renal plasma flow and urine productionwere greater than in normocapnia, and renal vascular resistancewas decreased greatly compared with normocapnia. There was littlechange in glomerular filtration rate.     

THE EFFECTS OF ANAESTHESIA WITH THIOPENTONE, NITROUS OXIDE, NARCOTICS AND NEUROMUSCULAR BLOCKING DRUGS ON RENAL FUNCTION IN NORMAL MAN

Changes in renal haemodynamics, water and electrolyte excretionwere determined in 10 healthy male volunteers before and afterthe administration of narcotic and atropine sulphate intravenously,and after anaesthesia with thiopentone, nitrous oxide in oxygen,neuromuscular blocking drugs and in some instances intermittentnarcotic. A significant reduction in glomerular filtration rate(13 per cent) without change in renal plasma flow with an increasedrenal vascular resistance was observed following narcotic andatropine premedication. No alteration in urine volume or osmolalityfollowed narcotic premedication suggesting failure of ADH release.Administration of anaesthesia resulted in a further reduction(11 per cent) in glomerular filtration rate, a 31 per cent reductionin renal plasma flow and maintained increase in renal vascularresistance. A profound antidiuresis characterized by low urinevolume, increased urine osmolality, and negative free waterclearance was observed during anaesthesia. This could not bereversed by ethanol infusion, unlike the response in previousstudies with cyclopropane and halothane. ^*Present address: Michael Reese Hospital andMedical Center,Chicago, Illinois 60616.     

阻塞性黄疸患者手术前后内毒素、内皮素及细胞因子水平的研究

目的 探讨阻塞性黄疸手术前后内毒素（LPS）、内皮素（ET）、TNF－α、IL-6及IL－8的变化。方法 观察15例阻塞性黄疸（OJ组）和15例无黄疸的肝胆外科患者（NOJ组）上述各指标的变化。结果 两组在各时段（术前及术后1、4、7天）上述指标差异均有显著性意义（P＜0．05）。OJ组术后1天各项指标均有升高，NOJ组患者术后1、4、7天变化不明显。结论 OJ组术后LPS、ET、TNF-α、IL－6及IL－8均升高，且在多脏器功能损害中起到重要作用，其损害的机理有待进一步研究。