8例急性呼吸窘迫综合征的误诊分析

８例急性呼吸窘迫综合征的误诊分析王纯王晋明许家王利急性呼吸窘迫综合征（ＡＲＤＳ）与急性左心衰竭（左心衰）均为临床急危重症，两者在发病特点、临床表现上有许多相似之处，临床上常有误诊发生。现就临床所见８例误诊情况，分析如下。１临床资料１．１病例：男５例，...     

无创通气在早期急性呼吸窘迫综合征治疗中的作用

急性呼吸窘迫综合征 (ARDS)是一个弥漫性的严重肺损伤综合征 ,近年来 ,一些学者认为它不仅是多脏器功能衰竭(MODS)的肺部表现 ,更可能是其起动因子 ,因此对 ARDS的早期诊断和治疗尤为重要。随着无创正压通气技术在临床的广泛应用 ,使 ARDS的早期治疗成为可能 ,本文通过比较我院自1998- 0 8～ 2 0 0 0 - 0 8间应用双水平无创正压通气 (BIPAP)和经典有创通气治疗 ARDS,总结无创正压通气在早期 ARDS治疗中的作用。1　对象和方法资料来自我院病案室 ,共计 8例 ,其中 5例应用 BIPAP,3例应用有创通气。ARDS的诊断符合 1999年全国…     

急性呼吸窘迫综合征的动物模型

急性呼吸窘迫综合征（ＡＲＤＳ）系多种原发疾病如休克、创伤、严重感染、误吸等疾病过程中发生的急性进行性缺氧性呼吸衰竭。其主要病理生理改变为弥漫性肺损伤、肺微血管壁通透性增加和肺泡群萎陷，导致肺内血液分流增加和通气／血流比失衡，临床表现为严重的不易缓解的...     

急性呼吸窘迫综合征的新进展

一、关于急性呼吸窘迫综合征 (ＡＲＤＳ)定义及诊断标准的进展成人呼吸窘迫综合征 (Ａｄｕｌｔｒｅｓｐｉｒａｔｏｙｄｉｓｔｒｅｓｓｓｙｎｄｒｏｍｅ ,ＡＲＤＳ)的命名起自 1971年 ,沿用了 2 0年。 1992年美国胸病学会 (ＡＴＳ)和欧洲危重病学会 (ＥＳＩＣＭ)联合召开讨论会 ,共同建议将ＡＲＤＳ中的Ａ改为Ａｃｕｔｅ (急性 ) ,并建议将该综合征划分为急性肺损伤(Ａｃｕｔｅｌｕｎｇｉｎｊｕｒｙ ,ＡＬＩ)和ＡＲＤＳ (ａｃｕｔｅｒｅｓｐｉｒａｔｏｒｙｄｉｓｔｒｅｓｓｓｙｎｄｒｏｍｅ,ＡＲＤＳ)两部分 ,前者反映该综合征的病生理过程 ,…     

急性呼吸窘迫综合征

急性呼吸窘迫综合征(ARDS)是一组继发于内外科疾患的以急性肺损伤为特征的临床综合征，本文就ARDS的定义、临床特征、流行病学特点以及发病机制方面的进展作一综述。     

急性呼吸窘迫综合征临床治疗进展

急性呼吸窘迫综合征（ＡＲＤＳ）至今仍缺乏特殊治疗方法,绝大部分措施仍属于支持治疗。本文就ＡＲＤＳ的治疗进展作一综述。１　ＡＲＤＳ的非药物治疗１．１　体位〔１３〕：由于ＡＲＤＳ的肺浸润不均匀性,改变体位可以改善通气。在理论上浸润较轻的区域通气和灌注更为有效。俯卧位的作用最为显著,经２小时俯卧位改善气体交换的疗效甚至可持续到恢复为仰卧位后。严重创伤患者早期应用体位预防性治疗可降低ＡＲＤＳ、肺炎的发生率和病死率。适应证包括：急性肺损伤、心源性肺水肿和渗透性肺水肿;禁忌证有急性出血、多发性创伤、脊椎损伤…     

关于急性呼吸窘迫综合征的诊断

通过对１７例急性感染患者资料分析，从急性呼吸窘迫综合征（ＡＲＤＳ）的发展过程探讨其诊断，特别是早期诊断。     

急性肺损伤和急性呼吸窘迫综合征的支持治疗

急性呼吸窘迫综合征（ＡＲＤＳ）至今仍缺乏有效治疗,与其相关的病死率仍在５０％以上〔１〕。目前治疗ＡＲＤＳ及急性肺损伤（ＡＬＩ）的一般原则包括：治疗导致ＡＲＤＳ和ＡＬＩ的基础疾病,排除感染因素（所有ＡＬＩ和ＡＲＤＳ的患者,都应该怀疑有感染）,除外弥散性肺炎（一般要求用支气管镜、支气管肺泡灌洗、经支气管肺活检３种方法排除）,支持治疗（包括机械通气、体位治疗、血流动力学管理、血管活性药物的应用、实验性药物治疗、继发性并发症的防治等）。其中支持治疗仍是治疗的关键和重点。本文就有关ＡＬＩ和ＡＲＤＳ的支持治…     

急性呼吸窘迫综合征——努力提高急性呼吸窘迫综合征的诊治水平

1 引 言 急性呼吸窘迫综合征acute respiratory distress syndrome，ARDS是以通气／血流灌注比例严重失调为主要特征的急性、进行性、缺氧性呼吸衰竭。自1967年Ashbaugh首次报告以后，世界各国医学界都非常重视本综合征。有关ARDS在我国的发病率尚无精确统计。美国每年约有150 000例。ARDS比较多见于内科、外科、妇产科的危重病例，往往在各种类型休克、严重感染、严重创伤的抢救过程中发生。尽管目前对其认识和治疗措施有很大进展，对早期病例抢救成功率提高，但病死率仍很高，达40％至60％。2 ARDS的发病机制 ARDS的发病机制…     

血管性假血友病因子和细胞间黏附分子-1在急性呼吸窘迫综合征中的动态变化及早期诊断的意义

目的检测血管性假血友病因子、可溶性细胞间黏附分子-1浓度变化，以研究其在ARDS早期诊断中的意义。方法以ELISA法检测非ARDS组和ARDS组于0、2、3、5和7d血浆vWF和slCAM-l浓度。结果ARDS组vWF和sICAM-1浓度高于非ARDS组，前四个时点的中性粒细胞活化计数ARDS组高于非ARDS组。血浆vWF和sICAM-1水平具有相关性。结论血浆vWF和sICAM-1浓度及中性粒细胞活化计数在ARDS的早期即升高，对ARDS早期诊断有预警作用。     

血管内皮生长因子及炎性因子在油酸性犬急性呼吸窘迫综合征中的变化

目的探讨油酸性急性呼吸窘迫综合征（ARDS）beagle犬血浆及肺泡灌洗液血管内皮生长因子（VEGF）、可溶性细胞间黏附分子-1（ICAM-1）、白细胞介素-8（IL-8）、肿瘤坏死因子-α（TNF—α）水平的改变。方法12只英国纯种beagle犬，静脉注射油酸0．15mL／kg，在注射油酸前、后1h，出现ARDS的典型表现时，抽血测VEGF、sICAM-1、IL-8、TNF—α，并对此时相作肺泡灌洗液VEGF、sICAM—1、IL-8、TNF-α的测定。结果beagle犬静脉注射油酸后1h血浆TNF—α升高（P〈0．05），血浆反肺泡灌洗液IL8、sICAM-1和VEGF在1h较油酸前没有明显变化（P〉0．05），beagle犬油酸型ARDS模型建立后血浆及肺泡灌洗液VECF、sICAM-1、IL-8、TNF—α均显著高于建模前（P〈0．05）。结论VEGF、sICAM-1、IL-8、TNF～α在beagle犬油酸型ARDS发生发展过程中可能均起重要作用，其水平的高低可能与ARDS严重程度及预后有关。     

大鼠骨髓间充质干细胞血管细胞黏附分子1及细胞间黏附分子1的表达(英文)

背景:骨髓间充质干细胞系统性输注后,何种因素促使其迁移到正确部位尤为关键,目前认为黏附分子在介导骨髓间充质干细胞向缺血或损伤组织迁移过程中起重要作用.目的:观察血管细胞黏附分子1与细胞间黏附分子1在大鼠骨髓间充质干细胞中的表达.方法:采用直接贴壁法体外分离培养大鼠骨髓间充质干细胞,免疫细胞化学染色检测血管细胞黏附分子1及细胞间黏附分子1蛋白的表达,应用免疫荧光直标法在流式细胞仪上检测血管细胞黏附分子1及细胞间黏附分子1抗原的表达率,RT-PCR半定量分析血管细胞黏附分子1及细胞间黏附分子1 mRNA的表达.结果与结论:免疫细胞化学染色结果显示,骨髓间充质干细胞血管细胞黏附分子1呈弱阳性表达,细胞间黏附分子1呈强阳性表达.流式细胞仪检测结果显示,血管细胞黏附分子1表达率为6%,细胞间黏附分子1表达率为100%.RT-PCR检测结果显示,血管细胞黏附分子1 mRNA呈微弱表达,细胞间黏附分子1 mRNA呈高度表达.提示在生理状态下,体外培养的大鼠骨髓间充质干细胞低表达血管细胞黏附分子1,高表达细胞间黏附分子1.     

Modulation of soluble phases of endothelial/leukocyte adhesion molecule 1, intercellular adhesion molecule 1, and vascular cell adhesion molecule 1 with interleukin-1beta after experimental endotoxic challenge

OBJECTIVE: To evaluate the effect of treatment with interleukin 1beta (IL-1beta) on the concentrations of soluble adhesion molecules after an endotoxic challenge. DESIGN: Randomized, controlled study. SETTING: Experimental Unit, Virgen de las Nieves University Hospital. SUBJECTS: Seventy-two female CBA/H mice of 20 to 21 g, supplied by the animal center of the Experimental Unit. INTERVENTION: The mice were randomized into three groups of 24. Group 1 (sham) received two intraperitoneal (ip) doses of 0.1 mL of phosphate-buffered saline; group 2 (lipopolysaccharide) was injected with 125 mg/kg lipopolysaccharide (Escherichia coli) (i.p.) 24 hrs after 0.1 mL of phosphate-buffered saline; group 3 was pretreated with 80 ng (i.p.) of IL-1beta per mouse 24 hrs before the endotoxic challenge. MEASUREMENTS AND MAIN RESULTS: At 1, 2, 4, and 24 hrs after the endotoxic challenge, the concentrations of soluble endothelial/leukocyte adhesion molecule 1 (ELAM-1), intercellular adhesion molecule 1 (ICAM-1), and vascular cell adhesion molecule 1 (VCAM-1) were measured in the three groups. There was a significant increase (p <.01) in these concentrations at these times in comparison with the sham group. The use of IL-1beta produced a significant decrease (p <.05) in the three molecules among the treated group versus the group submitted only to the challenge; concentrations of ELAM-1 significantly decreased to below those of the sham group, and those of VCAM-1 reduced to levels that did not significantly differ from those of the sham group. CONCLUSION: Endotoxin administration significantly increases the concentrations of soluble ELAM-1, ICAM-1, and VCAM-1 in mice. Treatment with IL-1beta significantly decreases these concentrations, probably attenuating cell injury and organ dysfunction.     

长链非编码RNAs在急性呼吸窘迫综合征中的作用

急性呼吸窘迫综合征(ARDS)是以顽固性低氧血症为特征的临床常见危重综合征,免疫炎症反应失衡、氧化应激和内皮功能障碍在其中发挥了重要作用。长链非编码RNAs(lncRNAs)可通过调控细胞核的结构和转录以及调节细胞质中的mRNA稳定性、转录和翻译后修饰,进而调控机体免疫炎症等信号转导网络,参与ARDS发生发展过程。该文综述lncRNAs在ARDS临床研究中的新发现及其在免疫炎症反应、血管内皮损伤及组织修复等ARDS病理过程中的作用。     

阿托伐汀对急性冠状动脉综合征患者血清可溶性细胞间黏附分子-1和可溶性血管细胞黏附分子-1的影响--附68例检测结果分析

目的:观察早期应用阿托伐汀对急性冠状动脉综合征患者的可溶性细胞间黏附分子-1(soluble intercellular adhesion molecules-1,sICAM-1)和可溶性血管细胞黏附分子-1(soluble vascularcell adhesion molecules-1,sVCAM-1)的影响,探讨阿托伐汀降低急性冠状动脉综合征炎症反应的可能机制.方法:稳定型心绞痛30例,急性冠状动脉综合征68例,后者再分为两亚组:阿托伐汀组35例,非阿托伐汀组33例.用酶联免疫吸附法测定急性冠状动脉综合征患者入院后第1、3、5、7、14日的sICAM-1和sVCAM-1水平,观察阿托伐汀对其sICAM-1和sVCAM-1水平的影响.结果:急性冠状动脉综合征患者入院时血清sICAM-1和sVCAM-1水平均比稳定型心绞痛组明显增高(P＜0.01).治疗后急性冠状动脉综合征两亚组的血清sICAM-1和sVCAM-1水平均有不同程度的降低,其中阿托伐汀组的下降更显著.结论:阿托伐汀可以降低炎症反应,在急性冠状动脉综合征的早期治疗中起重要作用.     

Soluble intercellular adhesion molecule, vascular cell adhesion molecule, and impaired microvascular reactivity are early markers of vasculopathy in type 2 diabetic individuals without microalbuminuria.

OBJECTIVE: Using von Willebrand Factor (vWF) as a marker of endothelial function, previous studies have shown that the development of microalbuminuria is associated with the onset of endothelial dysfunction in individuals with type 2 diabetes. We tested the hypothesis that endothelial dysfunction is already evident in normoalbuminuric individuals with type 2 diabetes. RESEARCH DESIGN AND METHODS: We used laser Doppler imaging scanning to measure vasodilation in the forearm skin in response to iontophoresis of 1% acetylcholine (endothelium-dependent) and 1% sodium nitroprusside (endothelium-independent). Multiple indicators of endothelial function--soluble intercellular adhesion molecule (sICAM), soluble vascular cell adhesion molecule (sVCAM), vWF, and microvascular reactivity--were measured in 20 healthy control subjects, 45 normoalbuminuric (urinary albumin/creatinine ratio < 30 micrograms/mg) individuals with type 2 diabetes, and 14 microalbuminuric (urinary albumin/creatinine ratio between 30 and 300 micrograms/mg) individuals with type 2 diabetes. RESULTS: Serum sICAM and sVCAM levels were elevated in the normoalbuminuric (305 +/- 120, 851 +/- 284 ng/ml) and microalbuminuric (300 +/- 89, 845 +/- 252 ng/ml) individuals with diabetes when compared with the healthy control subjects (213 +/- 58, 661 +/- 176 ng/ml) (P < 0.01). Furthermore, the microvascular endothelium-dependent and -independent vasodilation was reduced in the normoalbuminuric (76 +/- 44, 70 +/- 33) (percent increase in perfusion over baseline) and microalbuminuric (74 +/- 41, 73 +/- 28) individuals with diabetes compared with healthy control subjects (126 +/- 67, 120 +/- 47) (P < 0.05). In contrast, plasma vWF was elevated only in the microalbuminuric individuals with diabetes (129 +/- 35%) compared with the normoalbuminuric individuals with diabetes (110 +/- 34) and healthy control subjects (111.3 +/- 39) (P < 0.05). On stepwise multivariate analysis, fasting blood glucose was the most important contributing factor to the variation in microvascular reactivity and sVCAM, whereas insulin resistance (by homeostasis model assessment) was the most important contributing factor to the variation in sICAM. Addition of all clinical and biochemical measures explained only 15-22% of the variation in sICAM, sVCAM, and microvascular reactivity. CONCLUSIONS: Multiple markers of endothelial dysfunction were evident in normoalbuminuric individuals with type 2 diabetes. The pathogenic process of vasculopathy in type 2 diabetes occurs early and may be operative before the development of microalbuminuria.     

The acute respiratory distress syndrome

The acute respiratory distress syndrome (ARDS) is an important cause of acute respiratory failure that is often associated with multiple organ failure. Several clinical disorders can precipitate ARDS, including pneumonia, sepsis, aspiration of gastric contents, and major trauma. Physiologically, ARDS is characterized by increased permeability pulmonary edema, severe arterial hypoxemia, and impaired carbon dioxide excretion. Based on both experimental and clinical studies, progress has been made in understanding the mechanisms responsible for the pathogenesis and the resolution of lung injury, including the contribution of environmental and genetic factors. Improved survival has been achieved with the use of lung-protective ventilation. Future progress will depend on developing novel therapeutics that can facilitate and enhance lung repair.     

Human vascular endothelial cell adhesion receptors for Plasmodium falciparum-infected erythrocytes: roles for endothelial leukocyte adhesion molecule 1 and vascular cell adhesion molecule 1

The clinical complications associated with severe and cerebral malaria occur as a result of the intravascular mechanical obstruction of erythrocytes infected with the asexual stages of the parasite, Plasmodium falciparum. We now report that a primary P. falciparum-infected erythrocyte (parasitized red blood cell [PRBC]) isolate from a patient with severe complicated malaria binds to cytokine-induced human vascular endothelial cells, and that this adhesion is in part mediated by endothelial leukocyte adhesion molecule 1 (ELAM-1) and vascular cell adhesion molecule 1 (VCAM-1). PRBC binding to tumor necrosis factor alpha (TNF-alpha)-activated human vascular endothelial cells is partially inhibited by antibodies to ELAM-1 and ICAM-1 and the inhibitory effects of these antibodies is additive. PRBCs selected in vitro by sequential panning on purified adhesion molecules bind concurrently to recombinant soluble ELAM-1 and VCAM-1, and to two previously identified endothelial cell receptors for PRBCs, ICAM-1, and CD36. Post-mortem brain tissue from patients who died from cerebral malaria expressed multiple cell adhesion molecules including ELAM-1 and VCAM-1 on cerebral microvascular endothelium not expressed in brains of individuals who died from other causes. These results ascribe novel pathological functions for both ELAM-1 and VCAM-1 and may help delineate alternative adhesion pathways PRBCs use to modify malaria pathology.     

细胞外囊泡在急性呼吸窘迫综合征中潜在作用的研究进展

急性呼吸窘迫综合征（ARDS）是由肺和肺外多种损伤引起的危及生命的疾病,其病死率居高不下,发病机制仍需进一步阐明。近些年的研究表明,失衡的免疫应答在ARDS的发生发展中起重要作用。细胞外囊泡（EVs）是一种细胞分泌的小的无核细胞结构,可以在多种细胞类型间靶向转移多种生物物质,在细胞通讯及物质传递方面起重要作用。近年来对EVs的研究为阐明ARDS的发病机制及其治疗提供了新的思路。本文就EVs在ARDS中的潜在的生物标志物作用和治疗作用的研究进展作一综述,提出不同细胞来源的EVs可能作为ARDS早期识别的生物标志物以及临床治疗的新方向。