急性肺损伤早期抗凝疗法的研究

采用骨髓提取液静脉注射建立家兔急性肺损伤的动物模型。实验组在实验过程中使用肝素进行抗凝治疗，对照组不进行抗凝治疗。两组动物同时观察生命体征，血液气体分析，Ｘ线胸片，及肺病理学检查，分析早期抗凝疗法对急性肺损伤以及由此继发的全身脏器损害的影响。     

体外循环后急性肺损伤诊断与防治的研究进展

急性肺损伤是体外循环后的重要并发症之一 ,一氧化氮呼出水平下降、前降钙素水平的增加可提示急性肺损伤。体外循环后肺损伤的防治方法较多 ,如白细胞滤过术、抑制细胞因子、补体的活性、减轻全身炎症反应、持续肺灌流 ,液体通气 ,一氧化氮吸入治疗。但其疗效有待进一步评价。     

抗凝治疗——急性肺损伤/急性呼吸窘迫综合征治疗的新思路

急性肺损伤/急性呼吸窘迫综合征(ALI/ARDS)是指由心源性以外的各种肺内外致病因素导致的急性、进行性呼吸衰竭,以呼吸窘迫和低氧血症为特点,常需要机械通气治疗[1].     

急性肺损伤动物模型

急性肺损伤是临床常见的一种综合征,病死率较高。研究急性肺损伤的病理、生理过程,明确其发病机制,可为相关治疗策略提供指导和帮助。建立一种理想的急性肺损伤动物模型,有助于研究其发病机制。     

急性肺损伤动物模型

急性肺损伤是临床常见的一种综合征,病死率较高。研究急性肺损伤的病理、生理过程,明确其发病机制,可为相关治疗策略提供指导和帮助。建立一种理想的急性肺损伤动物模型,有助于研究其发病机制。     

促红细胞生成素在急性肺损伤与急性呼吸窘迫综合征中作用的研究进展

急性肺损伤（ALI）或急性呼吸窘迫综合征（ARDS）是临床常见急危重症。各种病因包括严重感染、创伤、休克、急性胰腺炎、肺炎等肺内或肺外因素均可导致ALI/ARDS,发病机制主要包括炎症反应、细胞凋亡、氧化应激和肺泡毛细血管膜的损害等,目前尚无特殊有效的治疗方法,临床上也无修复肺损伤的有效药物。促红细胞生成素（EPO）作为一种多功能的内源性调节因子对各种组织损伤有一定的细胞保护作用,尤其是肺组织〔1〕,成为治疗ALI/ARDS的研究热点,     

两种小儿急性肺损伤和急性呼吸窘迫综合征的分析

当前病理生理研究认为,引起急性肺损伤（ALI）及其危重阶段--急性呼吸窘迫综合征（ARDS）有两类病因：肺本身因素引起的直接肺损伤（ALI/ARDSp）;肺外因素引起的间接肺损伤（ALI/ARDSexp）.笔者就本院PICU自1996年以来收治的88例ALI/ARDSp和ALI/ARDS exp两组患儿作临床比较分析,现分析如下.     

急性肺损伤动物模型

急性肺损伤是临床常见的一种综合征,病死率较高。研究急性肺损伤的病理、生理过程,明确其发病机制,可为相关治疗策略提供指导和帮助。建立一种理想的急性肺损伤动物模型,有助于研究其发病机制。     

急性肺损伤生物标志物研究进展

急性肺损伤或急性呼吸窘迫综合征是呼吸系统危重病,表现为肺泡毛细血管通透性增加、肺间质水肿、炎性细胞浸润及肺部炎症损伤失控,病死率高。生物标志物可能成为急性肺损伤的预警指标。本文就急性肺损伤生物标志物的研究进展作一综述。     

血必净注射液对急性肺损伤大鼠氧自由基变化的影响

目的:探讨血必净注射液对急性肺损伤大鼠氧自由基变化的影响.方法:SD大鼠72只随机分为正常对照组、内毒素组(LPS组)和内毒素联合血必净组(LPS+XBJ组),后两组又分别分为给药后1、2、4、12 h 4个亚组,每个亚组8只.采用静脉注射LPS(5 mg/kg)建立急性肺损伤模型.LPS+XBJ组予静脉注射LPS后同时腹腔注射血必净(10 mL/kg),LPS组腹腔注射等量生理盐水(10 mL/kg),正常对照组给予等量生理盐水.观察各组肺组织病理学变化,检测各组肺湿干质量比(W/D)、血清丙二醛(MDA)浓度、超氧化物歧化酶(SOD)活力等的变化.结果:血必净注射液干预可显著降低急性肺损伤大鼠升高的W/D(P<0.05)和血清肺MDA浓度(P<0.01或P<0.05).显著升高急性肺损伤大鼠降低的SOD浓度(P<0.01或P<0.05),减轻肺组织形态学损伤.结论:血必净注射液可抑制氧自由基产生.对LPS所致急性肺损伤大鼠具有肺保护作用.     

IMMUNE MODULATION AND SEPSIS

The pathogenesis of sepsis involves not only microbial toxins but also activated host inflammatory mediators. Therefore, besides conventional antibiotic or surgical treatment of infection and supportive intensive therapy, modulating host inflammatory mediators as a conjunctive therapeutic option has been explored in the past decade. Although successful in animal models of sepsis, inhibiting host inflammatory response in human sepsis has failed to improve survival or otherwise show efficacy. Studies are needed which better describe the circumstances under which these therapies may ultimately prove successful.     

Toward resolving the challenges of sepsis diagnosis

Sepsis in the United States has an estimated annual healthcare cost of 16.7 billion dollars and leads to 120,000 deaths. Insufficient development in both medical diagnosis and treatment of sepsis has led to continued growth in reported cases of sepsis over the past two decades with little improvement in mortality statistics. Efforts over the last decade to improve diagnosis have unsuccessfully sought to identify a "magic bullet" proteic biomarker that provides high sensitivity and specificity for infectious inflammation. More recently, genetic methods have made tracking regulation of the genes responsible for these biomarkers possible, giving current research new direction in the search to understand how host immune response combats infection. Despite the breadth of research, inadequate treatment as a result of delayed diagnosis continues to affect approximately one fourth of septic patients. In this report we review past and present diagnostic methods for sepsis and their respective limitations, and discuss the requirements for more timely diagnosis as the next step in curtailing sepsis-related mortality. We also present a proposal toward revision of the current diagnostic paradigm to include real-time immune monitoring.     

脓毒症与铁代谢的研究进展

脓毒症是一种由感染引起的常见的全身炎症反应综合征,具有高发病率和高病死率的特征,已成为重要的公共健康问题之一。脓毒症及其发病机制和治疗也一直是研究重点。2016年,脓毒症被重新定义为由宿主对感染的反应失调引起的危及生命的器官功能障碍模式。近年来,针对脓毒症患者的免疫反应及代谢变化开展了大量临床及实验研究,其中铁代谢与脓毒症的关系也是研究重点之一。铁在调节免疫功能和微生物生长方面有着关键作用,已有研究证明铁代谢的变化会影响感染的风险。本文旨在对铁代谢与脓毒症及脓毒症诱导的多器官功能障碍的关系等作简要概述,以期对脓毒症的预后预测及治疗提供新的方向。     

感染诊疗应得到重视:支持美国感染病学会

Sepsis是导致重症患者死亡的重要原因。近年来,随着临床和基础研究的不断发展,人们对于Sepsis定义、诊断以及治疗认识不断深入,患者病死率持续下降。每4年颁布一次并更新的“拯救Sepsis运动(Surviving Sepsis Campaign,SSC)”指南受到国际广泛重视。2016年版SSC指南,在对Sepsis和感染性休克重新定义、重新制定诊断标准的基础上,于2017年1月正式发布。然而,2017年11月,美国感染病学会(Infectious Disease Society of America, IDSA)即在其官方期刊Clin Infect Dis发表公开声明,对2016年版SSC指南中关于感染诊疗的推荐意见提出质疑。本文站在IDSA的立场,尝试从Sepsis概念、诊断及治疗3个方面解读IDSA声明,探讨Sepsis中的“感染”问题。     

病毒性脓毒症的研究进展与启发

脓毒症是一种由宿主反应失调引起的危及生命器官功能障碍的感染,具有复杂的生理和病理变化^[1]。近年来,人们对脓毒症的研究取得了很大进展,但对不同类型病原体引起的脓毒症差异研究尚少,大多数是针对细菌性脓毒症的研究。随着新型冠状病毒(COVID-19)的暴发,病毒性脓毒症再次引起人们关注。因此,了解病毒性脓毒症的常见病毒类型、发病机制的主要特征、临床表现、诊断、治疗等方面,能进一步调整后续诊疗策略,改善患者预后状况,有效降低临床病死率。     

从脓毒症诊治观念变迁看肾上腺皮质激素的应用

脓毒症是病原微生物感染引发的危及生命的器官功能障碍。由于病理生理机制的复杂性，自1991年对其概念的界定以来，已历经3次重要修订，但仍难以形成广泛共识。特别是在拯救脓毒症运动背景下，脓毒症发病率和死亡率居高不下、特效药物匮乏以及诸多经验性救治措施难以奏效的严峻现实表明，脓毒症非病原依赖性瀑布样介质反应尚有广阔的探索空间。肾上腺作为神经-内分泌-免疫调控网络的重要效应器官，通过接驳中枢应激信号和局部微环境反应，以效应激素形式参与对脓毒症机体反应的非线性、复杂性调控。其功能障碍的早期识别、替代治疗以及在脓毒症机体紊乱内环境中的再认识，无疑是脓毒症诊治的核心环节之一。近30年来，针对肾上腺皮质激素的多项临床研究以及争议性推荐意见进一步凸显其重要价值。为此，笔者基于预测性、预防性、个体化、参与性的"4P"医学模式，立足转化医学视角，从脓毒症定义及其内涵的变化，分析肾上腺皮质激素的诊治价值，并从内源性和外源性肾上腺皮质激素角度，阐述脓毒症治疗中基于神经-内分泌-免疫网络的微环境调控理论，尝试从肾上腺皮质激素(种类、用量、单独和联合治疗、时间窗)分析脓毒症理论研究瓶颈与临床实践困惑，旨在为脓毒症的肾上腺皮质激素应用提供有益的借鉴和启示。     

Biomarkers of sepsis: clinically useful?

PURPOSE OF REVIEW: The purpose of this review is to indicate recent developments in biomarkers of sepsis and to evaluate their impact on clinical use. According to the 'surviving sepsis campaign,' diagnosis of sepsis and infection is urgent; early and specific treatment is most effective to reduce complications and to decrease mortality. RECENT FINDINGS: A variety of biomarkers of sepsis is presently available. The diagnostic spectrum of the various markers, however, is different. Some primarily indicate severity of inflammation (e.g. interleukin-6), others respond to infection, but do not indicate the host response well (endotoxin, lipoprotein binding protein, triggering receptor on myeloid cells). There are new markers with limited clinical experience, for example triggering receptor on myeloid cells or mid-pro atrial natriuretic peptide (Seristra, Brahms AG, Hennigsdorf, Germany). Procalcitonin is a well-established biomarker of sepsis that fulfills several criteria of clinical needs: it responds both to infection and severity of inflammation and thus has an impact on therapy. Recent studies indicate that antibiotic treatment can also be guided by procalcitonin. Further indications, including diagnosis of invasive bacterial infections and diagnosis of sepsis in neonates and children have been reported recently. SUMMARY: Recent data and cumulative analyses indicate that biomarkers of sepsis improve diagnosis of sepsis. However, only a few markers have impact on therapy and fulfill the clinical requirements. Procalcitonin is a well-established marker, indicating infection, sepsis, and progression to the more severe stages of the disease. Today, this biomarker should be in the diagnostic portfolio of an intensive care unit or emergency ward.     

Linezolid pharmacokinetics and pharmacodynamics in clinical treatment

Linezolid has been widely used in the treatment of Gram-positive infections for more than a decade. It is unique amongst antibiotics active against most multiply-resistant Gram-positive bacteria in that there is an oral preparation with 100% bioavailability and an extensive volume of distribution. This review examines pharmacokinetic data relating to linezolid use in different patient groups (obesity, enteral feeding, renal failure, neonates, and paediatrics) and in different clinical conditions (sepsis syndrome, skin and soft tissue infection, diabetic foot infection, pneumonia, bone and joint infection, infection of the central nervous system, eye infection, and neutropenic sepsis).     

Recent evolution of renal replacement therapy in the critically ill patient

The epidemiology of severe acute renal failure has dramatically changed in the past decade. Its leading cause is sepsis and the syndrome develops mostly in the intensive care unit as part of multiple organ dysfunction syndrome. After the significant improvements obtained from the mid 1970s to the mid 1990s, the past decade has seen a dramatic evolution in technology leading to new machines and new techniques for renal and multiple organ support. Extracorporeal therapies are now performed using adequate treatment doses, which have resulted in improved survival in the general population. At the same time, patients with sepsis seem to benefit from the use of increased doses, as in the case of high-volume hemofiltration or of increased membrane permeability and sorbents as in the case of continuous plasmafiltration adsorption. The humoral theory of sepsis and the peak concentration hypothesis have spurred a significant interest in the use of such extracorporeal therapies for renal support and possibly for the therapy of sepsis. Ongoing research and prospective studies will further elucidate the role of such therapies in this setting.     

Heme oxygenase-1-derived carbon monoxide enhances the host defense response to microbial sepsis in mice

Sepsis is characterized by a systemic response to severe infection. Although the inflammatory phase of sepsis helps eradicate the infection, it can have detrimental consequences if left unchecked. Therapy directed against inflammatory mediators of sepsis has shown little success and has the potential to impair innate antimicrobial defenses. Heme oxygenase-1 (HO-1) and the product of its enzymatic reaction, CO, have beneficial antiinflammatory properties, but little is known about their effects on microbial sepsis. Here, we have demonstrated that during microbial sepsis, HO-1-derived CO plays an important role in the antimicrobial process without inhibiting the inflammatory response. HO-1-deficient mice suffered exaggerated lethality from polymicrobial sepsis. Targeting HO-1 to SMCs and myofibroblasts of blood vessels and bowel ameliorated sepsis-induced death associated with Enterococcus faecalis, but not Escherichia coli, infection. The increase in HO-1 expression did not suppress circulating inflammatory cells or their accumulation at the site of injury but did enhance bacterial clearance by increasing phagocytosis and the endogenous antimicrobial response. Furthermore, injection of a CO-releasing molecule into WT mice increased phagocytosis and rescued HO-1-deficient mice from sepsis-induced lethality. These data advocate HO-1-derived CO as an important mediator of the host defense response to sepsis and suggest CO administration as a possible treatment for the disease.