抗氧化治疗在急性肺损伤和急性呼吸窘迫综合征中的应用进展

正急性肺损伤和急性呼吸窘迫综合征是由多种损伤因素导致的肺部的急性炎性损伤,这些损伤因素包括:严重的肺炎、脓毒血症、大量的输血和严重创伤等[1-2]。急性肺损伤和急性呼吸窘迫综合征是以急性起病、气体交换功能受损、肺顺应性降低和肺水肿形成为特点[3-4]。其中最主要的病理生理改变是肺毛细血管通透性的增加[5]。从1967年第一次报道至今,人们对急性肺损伤和急性呼吸窘迫综合征的病因、发展机制、临床表现和治疗方法进行了不懈的研究,但是其     

急性呼吸窘迫综合征患者实施俯卧位通气的护理难点及对策

<正>急性呼吸窘迫综合征(acute respiratiory distress syndrome,ARDS)多见于患者原心肺功能异常,由于肺外或肺内的严重疾病引起肺毛细血管炎症性损伤,通透性增加,继发急性高通透性肺水肿和     

急性肺损伤的发病机制:前B细胞集落增强因子是潜在的新靶点

急性肺损伤是临床常见的综合征,以炎症反应、肺血管通透性增加导致肺水肿、顽固性低氧血症、进展为急性呼吸窘迫综合征为主要病理特征.21世纪流感病毒再次大流行,急性期重症患者多有急性肺损伤表现,增加了阐明其发病机制的迫切性.研究认为前B细胞集落增强因子是一种新的炎症介质和急性肺损伤生物指标.现将近年对前B细胞集落增强因子在急...     

基质金属蛋白酶家族在急性肺损伤疾病发展过程中的作用

急性肺损伤（ALI）主要病理特征为肺毛细血管基底膜受损，导致微血管通透性增高，引起肺间质和肺泡渗出性肺水肿和透明膜形成，基质金属蛋白酶（MMPs）通过破坏基底膜、促进炎症过程中有关细胞的迁移以及细胞外基质（ECM）重建在ALI的发病过程中发挥重要作用。     

急性呼吸窘迫综合征时血管外肺水的检测方法及意义

急性呼吸窘迫综合征（ARDS）的本质是弥漫性肺泡毛细血管膜损伤、血管通透性增加所致的通透性肺水肿。血管外肺水（EVLW）的改变与肺水肿的程度具有高度相关性,EVLW作为预测、筛选ARDS患者以及反映ARDS患者病情、评价疗效和判断预后一个重要指标正在得到越来越广泛的的研究和使用。EVLW质和量的改变进行动态观察和定量检测,已成为呼吸窘迫综合综合征研究的热点,现就其检测方法和意义作一综述。     

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；     

急性肺损伤/急性呼吸窘迫综合征鼠类模型研究进展

急性肺损伤/急性呼吸窘迫综合征是现代危重医学的一大难题,发病机制尚未完全阐明.对急性肺损伤/急性呼吸窘迫综合征的很多研究是在动物急性肺损伤模型上进行的,根据致病因素研制模型,再根据模型研究其病理生理变化过程以及治疗方案.因此,急性肺损伤/急性呼吸窘迫综合征动物模型的制作一直是研究重点和热点.作者综述了目前急性肺损伤/急性呼吸窘迫综合征鼠类模型的研究现状.     

肺血管内皮细胞通透性与急性呼吸窘迫综合征

急性呼吸窘迫综合征（acute respiratory distress syndrome, ARDS）是广泛的肺泡上皮和毛细血管内皮损伤、内皮细胞通透性增加所致的渗透性肺水肿和顽同性低氧血症为特点的临床综合征,是危重症患者常见的一种并发症。     

肺血管内皮通透功能在急性肺损伤/急性呼吸窘迫综合征发病中的损伤机制

肺血管内皮功能损伤是急性肺损伤和急性呼吸窘迫综合征重要的病理表现之一.其特征为内皮通透性增加,引起肺间质水肿,患者临床症状为呼吸窘迫、低氧血症等.肺血管内皮通透功能损伤机制尚未完全阐明,目前认为主要是作用于内皮的致伤因子和保护因子的平衡失调.本文就肺血管内皮生理功能特征、通透性损伤机制及保护机制、临床治疗措施进行综述.     

急性呼吸窘迫综合征抢救成功1例

急性呼吸窘迫综合征(ARDS)是多发生于心肺功能正常患者,由于肺外或肺内的严重疾病引起毛细血管炎症性损伤,通透性增加继发急性高通透性肺水肿和进行性缺氧性呼吸衰竭(Ⅰ型)的一种临床综合征,呼吸窘迫综合征发病急、发展迅速,如不及时救治,很快呼吸衰竭而死亡,其病死率高达50%～80%以上,我科一位溺水后出现急性呼吸窘迫综合征抢救成功,现报道如下。患者,男性,26岁,农民,因癫痫发作溺水,呼吸困难4h入院,患者既往有癫痫病史5年,一直口服药控制病情(具体药名及剂量不详),平素自觉良好,4h前浇地时突然抽搐面部朝向水沟,遂被人救起,当时神志不清…     

肺血管通透性指数对急性肺水肿鉴别诊断价值初探

目的 探讨肺血管通透性指数(PVPI)在急性肺水肿鉴别诊断中的价值.方法 选2004年5月至2008年9月收住东南大学附属中大医院重症医学科,留置脉搏指示连续心排血量(PiCCO)导管,氧合指数[PaO2/吸入氧浓度(FiO2)]＜300 mm Hg(1 mm Hg=0.133 kPa)且血管外肺水指数(EVLWI)≥7 ml/kg的急性肺水肿患者,分为急性肺损伤(ALI)组和心源性肺水肿组,观察PVPI、胸腔内血容量指数(ITBVI)、肺血容量(PBV)、血管外肺水(EVLW)/胸腔内血容量(ITBV)在2组中的变化与差异.结果 (1)34例患者纳入研究,其中ALI 22例,心源性肺水肿12例;(2)ALI组PVPI为2.7±1.4,心源性肺水肿组为1.9±0.6,2组比较,P＜0.05.EVLWI、ITBVI在2组间差异无统计学意义(P＞0.05);(3)PVPI与EVLWI呈正相关(r=0.762,P=0.000),与PaO2/FiO2呈负相关(r=-0.478,P=0.012);(4)纳入患者中肺内原因ARDS 8例,肺外原因ARDS 5例,肺外原因ARDS患者PVPI、EVLW/ITBV和EVLWI显著高于肺内原因ARDS患者.结论 PVPI有助于对重症患者肺水肿类型的鉴别.

Abstract：

Objective To assess the value of pulmonary vascular permeability index in differentiating acute lung injury (ALI) from cardiac pulmonary edema. Methods Critically ill patients with acute pulmonary edema were included from May, 2004 to September, 2008. Patients were divided into two groups, the ALI group and the cardiac pulmonary edema group (C group). Pulmonary vascular permeability index (PVPI) , intrathoracic blood volume (ITBVI) were determined by pulse indicator continuous cardiac output(PiCCO) system. Results ( 1 ) Thirty-four patients were enrolled, 22 cases in ALI group and 12 cases in C group. (2) The PVPI in patients of ALI group (2.7 ± 1.4) was higher than that of C group (1.9 ±0.6 ;P＜0.05). EVLWI and ITBVI did not have the significant difference between the two groups (P ＞0. 05). (3) PVPI was positively correlated with EVLWI(r = 0. 762) , negatively correlated with PaO2/ FiO2(r= -0.478). (4)ARDS was diagnosed in 13 cases, including 8 pulmonary cause(ARDSp) and 5 extra-pulmonary cause ( ARDSexp). PVPI, EVLW/ITBV and EVLWI of patients with ARDSexp were obviously higher than those with ARDSp. Conclusions PVPI may be useful for differentiating the types of pulmonary edema in the critically ill.     

Pulmonary edema fluid from patients with acute lung injury augments in vitro alveolar epithelial repair by an IL-1beta-dependent mechanism

Efficient alveolar epithelial repair is crucial for the restoration of the injured alveolar epithelial barrier in patients with acute lung injury (ALI) and the acute respiratory distress syndrome (ARDS). We hypothesized that pulmonary edema fluid from patients with ALI /ARDS would inhibit alveolar epithelial repair as measured in an in vitro epithelial wound-repair model using the human alveolar epithelial-like cell line A549. In contrast to our initial hypothesis, pulmonary edema fluid from patients with ALI/ARDS increased alveolar epithelial repair by 33 +/- 3% compared with pooled plasma from healthy donors (p < 0.01). By contrast, the plasma and the pulmonary edema fluid from patients with hydrostatic pulmonary edema, and the plasma from patients with ALI/ARDS had similar effects on epithelial repair as pooled plasma from healthy donors. Inhibition of interleukin-1beta (IL-1beta) activity by IL-1 receptor antagonist reduced alveolar epithelial repair induced by ALI/ARDS edema fluid by 46 +/- 4% (p < 0.001), indicating that IL-1beta contributed significantly to the increased epithelial repair. In summary, pulmonary edema fluid collected early in the course of ALI/ARDS increased alveolar epithelial repair in vitro by an IL-1beta-dependent mechanism. These data demonstrate a novel role for IL-1beta in patients with ALI/ARDS, indicating that IL-1beta may promote repair of the injured alveolar epithelium.     

肺表面活性物质在急性肺损伤/急性呼吸窘迫综合征中的研究进展

急性肺损伤／急性呼吸窘迫综合征（ALI／ARES）时肺表面活性物质的成分、功能等均发生变化，研究这些变化对防治ALI／ARDS的发生、发展及预后，都有十分重要的意义。本文综述了肺表面活性物质在ALI／ARDS中的组成成分、代谢、功能改变以及治疗方面的研究进展，为该领域的深入研究提供参考。     

重组人促红细胞生成素对内毒素诱导的ALI/ARDS大鼠的干预作用

目的：观察重组人促红细胞生成素(rhEPO)对 ALI/ARDS大鼠模型肺部炎症及肺-毛细血管通透性的干预。方法24只雌性 SD大鼠随机分为正常对照组、ALI/ARDS组、EPO 低剂量组和 EPO 高剂量组。以腹腔注射内毒素进行造模,不同剂量的 rhEPO 进行干预。末次干预后收集BALF计数炎症细胞以及蛋白总量;计量肺湿/干重比;HE染色观察肺组织病理变化。结果与正常对照组比较,ALI/ARDS组肺组织病理损害严重,肺湿/干重比增加,BALF中白细胞总数、中性粒细胞、淋巴细胞以及蛋白总量均显著增加(P 值均<0.01);与 ALI/ARDS 组比较,EPO 低剂量组和EPO 高剂量组肺组织病理损害明显缓解,肺湿/干重比下降,BALF 中白细胞总数、中性粒细胞、淋巴细胞以及蛋白总量均显著下降(P值均<0.01),且 EPO 高剂量组效果优于 EPO 低剂量组(P <0.05或P<0.01)。结论 rhEPO 可以明显改善ALI/ARDS大鼠肺组织炎症水平,降低肺-毛细血管通透性,有效抑制 ALI/ARDS的发病进程。     

Future research directions in acute lung injury: summary of a National Heart,Lung, and Blood Institute working group

Acute lung injury (ALI) and its more severe form, the acute respiratory distress syndrome (ARDS), are syndromes of acute respiratory failure that result from acute pulmonary edema and inflammation. The development of ALI/ARDS is associated with several clinical disorders including direct pulmonary injury from pneumonia and aspiration as well as indirect pulmonary injury from trauma, sepsis, and other disorders such as acute pancreatitis and drug overdose. Although mortality from ALI/ARDS has decreased in the last decade, it remains high. Despite two major advances in treatment, low VT ventilation for ALI/ARDS and activated protein C for severe sepsis (the leading cause of ALI/ARDS), additional research is needed to develop specific treatments and improve understanding of the pathogenesis of these syndromes. The NHLBI convened a working group to develop specific recommendations for future ALI/ARDS research. Improved understanding of disease heterogeneity through use of evolving biologic, genomic, and genetic approaches should provide major new insights into pathogenesis of ALI. Cellular and molecular methods combined with animal and clinical studies should lead to further progress in the detection and treatment of this complex disease.     

Effective attenuation of endotoxin-induced acute lung injury by 2,3-diacetyloxybenzoic acid in two independent animal models

The pathology of acute lung injury (ALI) is often modeled in animal studies by the administration of lipopolysaccharide (LPS), which results in an endotoxemia with sequelae similar to that seen in acute respiratory distress syndrome (ARDS). Here we report the results of two studies designed to examine the efficacy of a novel agent, 2,3-diacetyloxybenzoic acid (2,3-DABA), in the treatment of LPS-induced ALI. In two separate animal models, 2,3-DABA was effective in significantly reducing lung microvascular permeability, a condition commonly seen in ARDS, which results in pulmonary edema and respiratory insufficiency. In each model, it is demonstrated that the mechanism by which 2,3-DABA exerts this effect occurs subsequent to the recruitment of neutrophils to the site of inflammation. Lung permeability was significantly decreased in both models by treatment with 2,3-DABA, suggesting that this agent, either alone or in combination therapy, may be useful in the treatment of ALI associated with ARDS.     

急性肺损伤主要生物标志物的研究进展

ALI和ARDS是由急性高渗性肺水肿引发的进行性缺氧性呼吸衰竭,有着较高的发病率和病死率。在过去十年中,大量研究在ALI患者的血浆和BALF中发现多种生物标志物,其在ALI的病理生理过程中发挥重要作用,它包括各类炎症介质、肺部各类细胞分泌的大分子以及凝血一纤溶系统相关酶类等。本文将回顾现有的主要ALI生物标志物的研究进展。     

Acute lung injury and acute respiratory distress syndrome: experimental and clinical investigations

Acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) can be associated with various disorders. Recent investigation has involved clinical studies in collaboration with clinical investigators and pathologists on the pathogenetic mechanisms of ALI or ARDS caused by various disorders. This literature review includes a brief historical retrospective of ALI/ARDS, the neurogenic pulmonary edema due to head injury, the long-term experimental studies and clinical investigations from our laboratory, the detrimental role of NO, the risk factors, and the possible pathogenetic mechanisms as well as therapeutic regimen for ALI/ARDS.     

血管生成素与急性肺损伤

急性肺损伤是由肺毛细血管通透性增高而致的肺水肿,表现为重力依赖性的不均匀实变性疾病,而近年来发现血管生成素家族在调节毛细血管通透性、抗炎及调节肺动脉高压方面具有重要作用,本文就近年来两者关系研究的最新进展加以综述.