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.     

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.     

The Alpha-Defensin Prosthetic Joint Infection Test Has Poor Validity for Native Knee Joint Infection

BackgroundThe alpha-defensin test known as Synovaure has been very effective in diagnosis of prosthetic joint infections (PJIs). Being able to easily and accurately differentiate septic and inflammatory arthropathies in native joints would improve diagnostic workup and management. We tested the ability of an alpha-defensin test to distinguish septic from inflammatory or crystalline arthropathy in the native knee.Methods40 native knee joint fluid specimens were tested with cell count, fluid analysis, and culture and alpha-defensin testing. We determined the sensitivity and specificity of the alpha-defensin test using culture-positive fluid as the gold standard for septic arthropathy and positive crystals as the gold standard for crystalline arthropathy.ResultsThe Synovasure PJI test had 100% specificity for septic arthritis coupled with a 28% false-positive rate when applied to native knee aspirations. False-positive rate was 5.3 times higher in patients with crystals found in the joint fluid.ConclusionAlpha-defensin testing, in the form of the Synovasure PJI test, has a high-false-positive rate when used to distinguish septic and inflammatory arthritis in the native knee joint. Future work will need to determine the sensitivity and specificity of the newer native joint panel. Clinicians should be cognizant of the specific alpha-defensin test used when sampling native knee synovial fluid.     

内皮素与新生儿败血性休克的研究

为了探讨内皮素在新生儿败血性休克中的作用，应用体外培养及放射免疫测定法，观察内毒素对人脐静脉血内皮细胞分泌内皮素的影响及山莨菪碱（６５４－２）的可能作用，并测定３２例败血症及２１例败血性休克新生儿血浆内皮素含量的变化。结果：（１）内毒素能刺激人脐静脉内皮细胞内皮素的分泌，呈时间及剂量依赖性；（２）６５４－２在体外能抑制内毒素刺激的内皮素的合成；（３）新生儿败血症及败血性休克时血浆内皮素水平明显增高，并与疾病严重程度及预后有关。提示：内皮素参与新生儿败血性休克的病理生理过程，为６５４－２治疗败血性休克提供了新的理论依据。     

The risk of suicide in patients with critical illness: A population-based study in Taiwan

The authors investigated retrospectively the association between critical illness and risk of suicide attempts. The data are from Taiwan’s National Health Insurance Research Database. Propensity score matching, multivariable models, Kaplan–Meier analysis, and competing risk analysis were used to explore this association. The authors found that patients having an critical illness were associated with increased risk of suicide attempts after adjusting for risk factors (adjusted hazard ratio = 2.98; 95% confidence interval = 1.46–6.08). Among different subtypes of critical illness, patients with sepsis/septic shock exhibited the highest risk of suicide attempts (adjusted hazard ratio = 3.43, 95% confidence interval = 1.52–7.74). An association between critical illness and suicide attempts was shown. Sepsis/septic shock was found to confer the highest risk in these specific population.