乌司他丁辅助治疗重症感染性休克的价值分析

目的探究临床用乌司他丁辅助治疗重症感染性休克的治疗效果。方法90例重症感染性休克患者,随机分为观察组与对照组,每组45例。对照组患者采用西医常规治疗,观察组患者在对照组基础上联合乌司他丁治疗。比较两组患者治疗效果、体温情况、感染情况以及治疗前后白细胞计数、白细胞介素-6(IL-6)水平、格拉斯哥昏迷量表(GCS)评分、急性生理功能和慢性健康状况评分系统Ⅱ(APACHEⅡ)评分。结果治疗后,观察组白细胞计数(7.34±1.32)×10^9/L低于对照组的(9.41±1.16)×10^9/L,差异具有统计学意义(P<0.05)。治疗后,观察组高热、感染体征发生率分别为97.78%、86.67%,均高于对照组的82.22%、62.22%,差异具有统计学意义(P<0.05);观察组体温恢复时间、感染消失时间分别为(7.19±1.39)、(3.88±0.89)d,均短于对照组的(9.81±1.88)、(10.76±1.57)d,差异具有统计学意义(P<0.05)。观察组患者血清IL-6为(4.27±0.95)μg/L低于对照组的(9.58±1.07)μg/L,差异具有统计学意义(P<0.05)。观察组患者GCS评分和APACHEⅡ评分较治疗前均有所改善,GCS评分(8.19±1.59)分、APACHEⅡ评分(8.83±0.82)分均优于对照组的(6.81±1.82)、(14.71±3.52)分,差异均具有统计学意义(P<0.05)。观察组患者治疗总有效率95.56%明显高于对照组的77.78%,差异具有统计学意义(χ^2=6.154,P<0.05)。结论乌司他丁具有较好的抗炎效果,与西医治疗相结合可以提高临床疗效,加快重症感染性休克患者退热速度,缩短感染时间,降低白细胞计数及血清IL-6水平,改善GCS评分和APACHEⅡ评分,临床疗效较好。     

盲肠结扎穿刺致豚鼠急性肺损伤动物模型建立

目的 研究败血性急性肺损伤的动物模型，并探讨其在急性肺损伤研究中的意义。方法 用盲肠结扎穿刺(CLP)法的豚鼠急性肺损伤模型，结合动脉血气分析、外周血白细胞计数、肺湿重／干重比值(W／D)及肺组织病理观察。结果 CLP模型中动物的症状和表现缓慢出现，逐渐恶化．最后导致败血性休克，于2d左右出现大量死亡。结论 用盲肠结扎穿刺的方法制作豚鼠急性肺损伤动物模型较大鼠内毒素性休克，表现更类似于人类的肠源性肺损伤，且症状缓慢发生，逐渐恶化，有利于观察和进行各种干预。     

感染性休克早期目标指导性治疗方案的应用体会

目的 为加强外科围手术期处理，观察应用早期目标指导性治疗方案（early goal directed therapy，EGDT）对感染性休克患者的救治效果。方法 运用EGDT使入ICU8h内的感染性休克患者的中心静脉压（CVP）、平均动脉压（MAP）和上腔静脉血氧饱和度（ScvO2）达标。结果 本组20例感染性休克患者，在8h内CVP达标20例，MAP达标20例，ScvO2达标16例。结论 应用EDGT治疗感染性休克有较好的理论基础和实用性，在限定的时间内使所有的目标值达标存在一定的困难。     

The peri‐microvascular edema in hippocampal CA1 area in a rat model of sepsis

Encephalopathy is a common complication of sepsis. However, little is known about the morphological changes that occur in the brain during sepsis. In this study, fecal peritonitis was induced in Wistar rats, which had been monitored for 4 h before their brains were removed and samples from the CA1 area taken. In addition to higher blood pressure with a decreasing pattern and a significant drop in rectal temperature, an increased heart rate and marked respiratory failure were observed. The tissue was investigated and compared with corresponding hippocampal samples taken from sham‐operated and not operated control groups. Significantly more peri‐microvascular edema was found in the hippocampal CA1 area in the septic group. The percentages of the peri‐microvascular edema were 158.57 ± 3.6%, 122.84 ± 1.5% and 120.24 ± 1.9% in the fecal peritonitis group, sham‐operated and not operated control groups, respectively. The results may suggest that the edema observed around the microvessels may participate in the pathogenesis of the septic encephalopathy probably by causing in the microvascular permeability characteristics.     

感染性休克患者的负液体平衡与预后的关系

目的探究感染性休克治疗的前3天患者的液体平衡状态与预后的关系。方法采用回顾性对照研究。查看1999年1月至2003年12月收入首都医科大学附属复兴医院ICU的感染性休克患者病例记录,入选病例必须严格符合感染性休克的诊断标准,且既往无肾功能不全病史。采集病例相关数据以及诊断后第1、2、3天的液体平衡值。比较不同组别患者的急性生理和慢性健康评分(APACHEⅡ)、继发器官衰竭评分(SOFA)、液体平衡和病死率等数据。对影响患者预后的独立危险因素进行Logistic回归分析,确定和描述感染性休克患者的预后与在前3天的液体复苏治疗中出现的负平衡((0mL)相关因素的关系。结果负液体平衡患者与未出现负液体平衡患者2组的病死率差异有统计学意义(52.4%vs87.5%,χ2=5.303,P=0.021)。通过对入组时患者年龄、APACHEⅡ评分、第1天和第3天SOFA评分和正负平衡等影响患者预后的独立危险因素Logistic回归分析,表明前3天的治疗中,若有1d出现负液体平衡即可成为影响患者预后的独立危险因素(P=0.035)。结论在感染性休克前3天的治疗中,若有1d出现液体平衡负值即可成为影响感染性休克患者预后的独立因素,对感染性休克的28d生存预后有较强的预测性。在前3天的治疗中出现液体平衡为负值((0mL)的感染性休克患者的生存率比液体平衡为正值的患者的28d生存率高。     

NO及NO合成酶与感染性休克

感染性休克病理生理学过程十分复杂。NO在其中的作用既具有有害的一面，同时也存在有利的一面。受内毒素、细胞因子等诱导，iNOS表达上调并产生大量NO，引起循环衰竭、组织细胞损伤以及通过调节炎症介质基因表达扩大全身炎症反应。另一方面，eNOS所产生的NO对机体具有保护作用。然而，感染性休克时，eNOS蛋白质合成及其功能受到损害，反而成为血管内皮功能失常、诱发多器官功能障碍的重要原因。     

败血症休克大鼠血管L-精氨酸/一氧化氮途径的变化

目的:观察败血症休克大鼠主动脉内膜、中膜和外膜一氧化氮合成途径的改变。方法:雄性Wistar大鼠盲肠结扎并穿孔复制败血症休克模型,分别测定假手术组、早期休克组和晚期休克组大鼠主动脉内膜、中膜和外膜的亚硝酸盐(NO^-₂)含量、一氧化氮合酶(NOS)活性及L-精氨酸(L-Arg)转运;免疫组化染色检测诱导型一氧化氮合酶(iNOS)在主动脉各层的分布。结果:早期及晚期败血症休克大鼠主动脉内膜产生的NO^-₂含量、NOS活性及L-Arg转运速率均低于假手术组,而中膜和外膜的NO^-₂、NOS活性及L-Arg转运速率则显著高于假手术组,外膜增加的程度尤为显著。免疫组织化学染色显示,败血症休克时血管中膜和外膜尤其是外膜iNOS阳性染色明显较强。结论:败血症休克时血管内膜NO合成受到抑制,而中膜和外膜NO合成显著增强,这一改变与休克状态下血管中L-Arg转运、iNOS表达及其活性的变化有关。     

内毒素休克时自由基对肝脏细胞和亚细胞器的损伤

本文探讨氧衍生的自由基在内毒素休克时对肝脏细胞和亚细胞的损伤作用。给大鼠静注内毒素(3mg/kg体重)0.5小时后,尽管肝组织MDA没有明显升高(P>0.05),但线粒体和溶酶体悬液中MDA以及肝组织、线粒体、溶酶体SOD较对照已明显升高(P<0.05)。休克后2小时,肝组织、线粒体、溶酶体MDA均显著升高(P<0.01～0.001),以后升高更甚(P<0.001)。线粒体、溶酶体SOD在休克后2小时明显下降(P<0.05),休克后4小时肝组织和亚细胞器SOD均明显受抑(P<0.01～0.001)。血浆,溶血液MDA、SOD和溶酶体酶在休克后均有程度不同的改变。实验结果表明氧衍生的自由基在内毒素休克时引起肝细胞和线粒体、溶酶体等亚细胞器的脂质过氧化损伤,而亚细胞器的损伤似乎早于组织损伤。     

Activation of the endothelium by IL-1 alpha and glucocorticoids results in major increase of complement C3 and factor B production and generation of C3a.

Constitutive secretion of complement C3 and factor B by the endothelial cell (EC) is lowered by therapeutic concentrations of glucocorticoids such as hydrocortisone or dexamethasone, whereas regulatory protein factor H production is increased by these hormones. In contrast, the proinflammatory cytokine IL-1 alpha has a stimulatory effect on C3 and factor B secretion by the endothelium and an inhibitory effect on factor H secretion. In this study, we examined the combined effect of IL-1 alpha and glucocorticoids on C3 and factor B expression by the endothelial cell. When dexamethasone or hydrocortisone were added to IL-1 alpha, significant potentialization of IL-1 alpha-induced stimulation of C3 and factor B production was observed, occurring at various concentrations of either stimuli. Dose-response experiments indicate that, in vitro, optimal concentrations are in the range of 10(-7) to 10(-5) M for dexamethasone and 50-200 U for IL-1 alpha. In contrast, dexamethasone counteracts, in an additive way, the inhibitory effect of IL-1 alpha on regulatory complement protein factor H production by EC. Such a potentialization between glucocorticoids and IL-1 alpha was not observed for another marker of endothelial activation, IL-1 alpha-induced stimulation of coagulation tissue factor expression. The association of glucocorticoids and IL-1 alpha therefore appears to be a specific and major stimulus for the secretion of complement C3 and factor B, two acute-phase proteins, by the endothelium. As a result of the in vitro endothelium stimulation by glucocorticoids and IL-1 alpha, C3a is generated in the vicinity of the endothelial cell. This study further suggests that complement activation, with its deleterious consequences, may result from the stimulation of endothelium in situations where high levels of IL-1 alpha and endogenous glucocorticoids coexist, such as in septic shock.