急性肺损伤-急性呼吸窘迫综合征机械通气治疗研究进展

急性肺损伤（acute lung injury，ALI）／急性呼吸窘迫综合征（acute respiratory distress syndrome，ARDS）是在严重感染、休克、创伤及烧伤等非心源性疾病过程中，肺毛细血管内皮细胞和肺泡上皮细胞损伤造成弥漫性肺间质及肺泡水肿，导致的急性低氧性呼吸功能不全或衰竭。以肺容积减少、肺顺应性降低、严重的通气／血流比例失调为病理生理特征，临床上表现为进行性低氧血症和呼吸窘迫，肺部影像学上表现为非均一性的渗出性病变。     

急性肺损伤与急性呼吸窘迫综合征的诊治研究进展

1967年Ashbaugh首先对急性肺损伤(acutelung injury,ALI)进行描述,它是指在严重感染、休克、创伤及烧伤等非心源性疾病过程中,肺毛细血管内皮细胞和肺泡上皮细胞损伤造成弥漫性肺间质及肺泡水肿,导致的急性低氧性呼吸功能不全或衰竭。     

急性肺损伤与炎性介质

急性肺损伤（Acutelunginjury,ALI）是指由非心源性的各种严重肺内外致病因素如严重感染、创伤、休克、中毒、弥漫性血管内凝血等导致的急性进行性加重的呼吸困难和难治性低氧血症。ALI进一步发展可演变成为急性呼吸窘迫综合征（Acut respiratory distress syndrome,ARDS）。ALI／ARDS是严重威胁人类健康的多发病和常见病,病死率可高达30％～40％。     

炎症细胞因子与急性呼吸窘迫综合征的研究进展

<正>急性呼吸窘迫综合征(acute respiratory distress syndrome,ARDS)是指非心源性的各种肺内外致病因素导致的严重的急性缺氧性呼吸衰竭,临床上表现主要以急性呼吸窘迫、顽固性低氧血症为特征,主要的病理特征是肺泡及肺血管内皮受损,肺微血管通透性增加,肺泡腔出现富含蛋白质的渗出液,导致肺水肿和肺透明膜的形成。其主要的病理生理特征是肺容积减少、肺的顺应性降低,进而肺通气/血流     

成人急性肺损伤和急性呼吸窘迫综合征患者的无创和有创通气治疗新进展

<正>急性肺损伤(ALI)和急性呼吸窘迫综合征(ARDS)是指心源性以外的各种肺内外致病因素所导致的急性进行性缺氧性呼吸衰竭,以肺容积减少、肺顺应性降低、严重的通气/血流比例失调为共同的病理生理特征。临床上表现为呼吸窘迫、顽固性低氧血症,肺部影像学上表现为非均一性的渗出性病变〔1〕。起病急、病情重、病死率高达31.0%～86.4%。随着人们对     

急性肺损伤／急性呼吸窘迫综合征的机械通气策略的再认识

急性呼吸窘迫综合征（ARDS）是指由心源性以外的各种肺内、外致病因素引起肺泡-毛细血管损伤为主的急性呼吸衰竭，属于急性肺损伤（ALI）的严重阶段。不同的病因直接损伤肺组织或通过炎症细胞、炎性介质和细胞因子介导的炎症反应，引起肺泡膜损伤、通透性增加和微血栓形成，损伤肺泡上皮，使表面活性物质减少或消失，产生肺水肿和肺不张，导致严重而顽固的低氧血症，可诱发多器官功能衰竭。其诊断标准目前多采用1994年欧美共识会议修订的标准：（1）有致病的高危因素；（2）急性起病、呼吸频数和（或）呼吸窘迫；     

内皮祖细胞治疗急性呼吸窘迫综合征的研究进展

正急性呼吸窘迫综合征(acute respiratory distress syndrome,ARDS)起病急,病情凶险,预后差,其病死率约在30%~40%,是现代急危重症医学中的一大难题[1-2]。ARDS是由非心源性的各种肺内外致病因素导致的以急性呼吸窘迫、顽固性低氧血症为主要临床特征的急性进行性低氧性呼吸功能不全或呼吸衰竭[3]。ARDS病理特征是肺泡上皮细     

老年肺损伤的机械通气治疗

急性肺损伤（acutelunginjury,ALI）和急性呼吸窘迫综合征（acuterespiratorydistresssyndrome,ARDS）多发生于原心肺功能正常的患者,是由于心源性以外的各种肺内、肺外致病因素引起的以肺泡一毛细血管炎症损伤为主的急性I型呼吸衰竭,为临床上常见的危重症之一。     

急性肺损伤与糖皮质激素受体的研究进展

急性肺损伤/急性呼吸窘迫综合征（acute lung injury/acute respiratory distress syndrome,ALI/ARDS）是指心源性以外的各种肺内外致病因素所致的毛细血管膜及肺泡内皮损伤导致肺水肿和肺不张,以呼吸窘迫和顽固性低氧血症为临床特点的呼吸衰竭。糖皮质激素（glucocorticoid,GC）可作用于ALI/ARDS的多个发病环节,早期可用于ALI/ARDS的治疗,但疗效差异很大,一直存在争议,具体机制尚未清楚。近年来认为GC治疗ALI/ARDS的疗效与其受体数量及亲和力之间存在一定的关系。为此,就ALI/ARDS与糖皮质激素受体（glucocorticoid receptor,GR）二者关系进行综述,对于阐明GR的作用机制以及提出激素治疗指征具有重要意义。     

肺开放／复张策略研究进展

广泛性、小灶性肺不张和肺泡萎陷是急性肺损伤(ALI)/急性呼吸窘迫综合征(ARDS)主要病理改变,也是引起肺容量减少、肺内分流(Qs/Qr)增加、顺应性下降和顽固性低氧血症的主要原因.     

State of knowledge of helminth fauna of freshwater fishes of Poland

A total 89 fish and lamprey species has been recorded from Polish freshwater habitats. Twenty-seven of them (30.3%) have not been surveyed for parasitic helminthes. Some of the latter fishes are either rare or not easily accessible. Other live only in specific habitats in scattered localities. An important obstacle for studying parasite faunas of some fishes may be their status on an endangered species. Among the non-surveyed fishes, are those which have been relatively recently introduced to Poland or migrated there on their own. The present paper attempts to review all hitherto not studied helminthologically fish species, their habitats, localities and current protection status.     

高血压降压治疗目标的再认识

根据传统的高血压水平的定义,1993年WHO高血压治疗指南提出血压控制目标为<140/90mm Hg(1mm Hg=0.133kPa),但是并非所有患者都必须将血压降至同一水平,而应根据患者情况进行个体化治疗。Framingham进行的一项长达10～12年的心血管事件研究发现,第5年后,正常上限血压[收缩压(SBP     

Lack of correlation of degree of villous atrophy with severity of clinical presentation of coeliac disease

BACKGROUND AND AIM: Both the clinical presentation and the degree of mucosal damage in coeliac disease vary greatly. In view of conflicting information as to whether the mode of presentation correlates with the degree of villous atrophy, we reviewed a large cohort of patients with coeliac disease. PATIENTS AND METHODS: We correlated mode of presentation (classical, diarrhoea predominant or atypical/silent) with histology of duodenal biopsies and examined their trends over time. RESULTS: The cohort consisted of 499 adults, mean age 44.1 years, 68% females. The majority had silent coeliac disease (56%) and total villous atrophy (65%). There was no correlation of mode of presentation with the degree of villous atrophy (p=0.25). Sixty-eight percent of females and 58% of males had a severe villous atrophy (p=0.052). There was a significant trend over time for a greater proportion of patients presenting as atypical/silent coeliac disease and having partial villous atrophy, though the majority still had total villous atrophy. CONCLUSIONS: Among our patients the degree of villous atrophy in duodenal biopsies did not correlate with the mode of presentation, indicating that factors other than the degree of villous atrophy must account for diarrhoea in coeliac disease.