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1.
目的 认识危重病儿出现全身炎症反应综合征(SIRS)所致的小儿急性呼吸窘迫综合征(ARDS)是急性肺损伤(ALI)的最严重后果。方法 对43例尸检肺脏符合ARDS病理改变的病案进行回顾性评分和临床分析。结果 导致ARDS的基础疾病复杂,除呼吸系统疾病外,更多见于其它系统的危重疾病。危重病儿出现SIRS而致ALI演变最严重的后果是ARDS。结论 危重病儿SIRS-ALI-ARDS-MODS是迅速发展的。ALI涵盖了呼吸功能不全至衰竭的全过程。ARDS是ALI最严重的后果,是导致死亡的最主要原因之一。  相似文献   

2.
急性肺损伤(ALI)是心源性以外的各种肺内、外致病因素所引起的急性炎症反应,表现为急性、进行性低氧性呼吸衰竭,最终严重阶段为急性呼吸窘迫综合征(ARDS),小儿急性呼吸窘迫综合征是儿科重症监护室(PICU)中病死率极高的危重病之一,我科于2004年至2005年参加全国小儿急性呼吸窘迫综合征协作组对小儿ALI/ARDS的流行病学进行研究,同时开展小儿ALI/ARDS机械通气下呼吸力学研究.  相似文献   

3.
王杰 《重庆医药》2009,38(15):1972-1975
急性肺损伤(ALI)和急性呼吸窘迫综合征(ARDS)是各种原因引起的肺实质弥漫性损害,以急性发展的双肺毛玻璃改变为特征。ALI/ARDs与脓毒症的发病机制相似,均涉及失控的宿主防御反应,其病理变化包括凝血系统增强、纤溶系统抑制。新的证据显示,恢复凝血纤溶系统平衡可能是ALI/ARDS的潜在治疗目标。本文主要综述研究ALI/ARDS中凝血纤溶病理生理学和药物治疗的进展。  相似文献   

4.
戢慧 《贵州医药》2012,36(8):755-758
急性肺损伤(acute lung injury,ALI)/急性呼吸窘迫综合征(acute respiratory distress syndrome,ARDS)指创伤、感染、休克等疾病导致的进行性缺氧性呼吸衰竭.病理特点是多型核中性粒细胞浸润、弥漫性肺泡上皮细胞损伤、肺出血水肿及透明膜形成.ALI/ARDS是临床常见危重症,病死率为26%~35%[妇.肺泡Ⅱ型上皮细胞(AEC-Ⅱ)是肺泡壁的重要组成部分,也是ALI/ARDS发生、发展的重要参与者,其凋亡在ALI/ARDS的发病机制中至关重要[2].  相似文献   

5.
《中国药房》2015,(23):3306-3308
目的:为糖皮质激素(GC)治疗急性肺损伤/急性呼吸窘迫综合征(ALI/ARDS)提供实践和理论依据。方法:查阅近5年来国内外相关文献,对GC治疗ALI/ARDS的基础研究、临床应用、抗炎机制等方面的进展进行归纳和总结。结果:共查阅到相关文献129篇,其中有效文献84篇。GC抗炎机制众多,药理作用广泛,对于治疗ALI/ARDS的效果褒贬不一,剂量-时间-效应关系尚不明确。结论:GC治疗ALI/ARDS的抗炎效果理论上是可行的,临床疗效可能更依赖的是医师针对患者的个体化治疗。  相似文献   

6.
急性肺损伤(ALI)和急性呼吸窘迫综合征(ARDS)发病机制复杂,病死率高,是临床常见的棘手的呼吸系统急危重症。各种肺内外因素引起多种炎症介质的释放,引发肺内过度、失控的炎性反应,形成恶性循环,使机体损伤加重。越来越多的证据表明,单核-巨噬细胞在ALI/ARDS发病中起着重要的作用。  相似文献   

7.
陈超  谷藏言  田惠玉 《河北医药》2012,34(16):2480-2481
急性肺损伤/急性呼吸窘迫综合征(ALI/ARDS)是由心源性以外的各种肺内外致病因素导致的急性、进行性缺氧性呼吸衰竭的一种疾病.ARDS发病机制错综复杂,目前尚未完全阐明,但已证明多种效应细胞释放的炎症介质是造成ARDS的"中心环节".本研究旨在探讨患者血清ICAM-1和CRP水平与ALI/ARDS严重程度的关系.  相似文献   

8.
乌司他丁治疗急性肺损伤的研究进展   总被引:4,自引:0,他引:4  
急性肺损伤和急性呼吸窘迫综合征是指由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。ALI是ARDS的早期阶段。早期、有效地治疗是防止ALI发展到ARDS的最佳时期。笔者对乌司他丁治疗ALI/ARDS的研究进行综述。  相似文献   

9.
急性肺损伤的药物治疗   总被引:2,自引:1,他引:2  
急性肺损伤(Acute lung injury,ALI)和急性呼吸窘迫综合征(Acute respiratory distress syndrome,ARDS)是指由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。ALI是ARDS的早期阶段。随着对ALI/ARDS发病机制研究的不断深入和临床综合治疗水平的进一步提高,使ALI/ARDS的病死率呈现下降趋势,但目前ALI/ARDS的病死率仍高于50%。  相似文献   

10.
失血性休克是急性肺损伤(acute lung injury.AU)和急性呼吸窘迫综合征(acute respiratory distress syndrome,ARDS)的病因之一。对其复苏不当可诱发和加重ALI/ARDS。高渗盐水因其快速、有效、低容量使用、不良反应小等特点。近年来在此类患者中的应用倍受关注。本文就高渗盐水对失血性休克急性肺损伤影响的可能机制和应用中存在的问题作如下综述。  相似文献   

11.
急性肺损伤(ALI)中炎症信号通路的失调控以及炎症因子平衡紊乱是其发生和发展的重要原因。能直接被cAMP活化的交换蛋白(Epac)在调节肺部气道炎症和细胞增殖方面是一个新的效应器,新的关于cAMP依赖性蛋白激酶A(PKA)非依赖性通路研究表明,cAMP/Epac/Rap1信号通路参与并行使许多类型细胞的功能,包括细胞分泌、细胞间黏附和连接、细胞凋亡、细胞增殖和分化等。cAMP能通过Epac/Rap1信号通路参与ALI的发病过程,Epac/Rap1信号通路是ALI防治的潜在靶点。本文综述Epac/Rap1信号通路在肺部相关炎症及急性肺损伤中作用机制的国内外研究进展。  相似文献   

12.
Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is an acute life-threatening form of hypoxemic respiratory failure with a high mortality rate, and there is still a great need for more effective therapies for such a severe and lethal disease. Dysfunction of endothelial and epithelial barriers is one of the most important mechanisms in hypoxia-associated ALI/ARDS. The acceleration of the epithelial repair process in the injured lung may provide an effective therapeutic target. KGF-2, a potent alveolar epithelial cell mitogen, plays an important role in organ morphogenesis and epithelial differentiation, and modulates a variety of mechanisms recognized to be important in alveolar repair and resolution in ALI/ARDS. Preclinical and clinical studies have suggested that KGF-2 may be the candidate of novel therapies for alveolar epithelial damage during ALI/ARDS.  相似文献   

13.
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are acute life-threatening forms of hypoxemic respiratory failure. ALI/ARDS patients require intensive care with prolonged mechanical ventilation. Despite advances in our understanding of the pathophysiology of ALI/ARDS, mortality rates remain > 30% and survivors suffer significant decrements in their quality of life. The evolving understanding of ALI/ARDS and the complex interactions involved in ALI/ARDS open the door for many potential targets for treatment. The condition is characterised by an acute inflammatory state that leads to increased capillary permeability and accumulation of proteinaceous pulmonary oedema. The changes that occur as a result of this inflammation clinically manifest themselves as hypoxemia, infiltrates on chest radiograph and reduced lung compliance. Many years have been dedicated to analysing the complexities involved in ALI/ARDS in order to improve current and future possibilities for treatment, with the aim of improving patient outcomes. Although some therapies have demonstrated benefits of improved oxygenation, such as surfactant and nitric oxide, these benefits have not translated into reductions in the duration of mechanical ventilation or mortality. Inflammatory mediator-targeted therapies were promising early on; however, larger trials have found therapies such as cytokine modulation, platelet-activating factor inhibition and neutrophil elastase inhibitors to be ineffective in the treatment of ALI/ARDS. Preclinical studies with β2-agonists and granulocyte macrophage colony-stimulating factor have shown promise for restoring alveolar capillary barrier integrity or reducing pulmonary oedema, and further studies are being conducted to test for true clinical benefit. Despite previous therapeutic failures, newer surfactant formulations have shown promise, particularly in patients with direct forms of lung injury, and are currently in Phase III trials. Anticoagulant therapy with activated protein C has been shown to improve survival in sepsis, the most common risk factor for the development of ALI/ARDS, and is now being studied in ALI/ARDS. Until new data emerge, the focus must remain on supportive care, including optimised mechanical ventilation, nutritional support, manipulation of fluid balance and prevention of intervening medical complications.  相似文献   

14.
Acute lung injury (ALI) and the acute respiratory distress syndrome (ARDS) are characterized by rapid-onset respiratory failure following a variety of direct and indirect insults to the parenchyma or vasculature of the lungs. Mortality from ALI/ARDS is substantial, and current therapy primarily emphasizes mechanical ventilation and judicial fluid management plus standard treatment of the initiating insult and any known underlying disease. Current pharmacotherapy for ALI/ARDS is not optimal, and there is a significant need for more effective medicinal chemical agents for use in these severe and lethal lung injury syndromes. To facilitate future chemical-based drug discovery research on new agent development, this paper reviews present pharmacotherapy for ALI/ARDS in the context of biological and biochemical drug activities. The complex lung injury pathophysiology of ALI/ARDS offers an array of possible targets for drug therapy, including inflammation, cell and tissue injury, vascular dysfunction, surfactant dysfunction, and oxidant injury. Added targets for pharmacotherapy outside the lungs may also be present, since multiorgan or systemic pathology is common in ALI/ARDS. The biological and physiological complexity of ALI/ARDS requires the consideration of combined-agent treatments in addition to single-agent therapies. A number of pharmacologic agents have been studied individually in ALI/ARDS, with limited or minimal success in improving survival. However, many of these agents have complementary biological/biochemical activities with the potential for synergy or additivity in combination therapy as discussed in this article.  相似文献   

15.
The acute respiratory distress syndrome (ARDS) is a severe form of acute lung injury (ALI). Its pathogenesis is closely linked with reactive oxygen species (ROS). Antioxidation has been considered as an efficient treatment. Besides, liposomes are widely investigated as potential drug carriers due to their ability to protect and carry drug molecules to the target organ such as the lung. The present study was undertaken to investigate whether dipyridamole (DIP), delivered as a liposomal preparation, can ameliorate the lipopolysaccharides (LPS)-induced ALI due to the changes of its biodistribution. First, the liposomes entrapping DIP were prepared by film hydration for treating ARDS. Subsequently, the characterizations including entrapment efficiency, size, span and micrograph of DIP liposomes were measured. The concentration change of DIP in tissues and plasma of mice after intravenous administration of DIP injection and DIP liposomes was determined by RP-HPLC and calculated to lung targeting parameters. To prove the therapeutic efficiency, the effects of DIP liposomes on LPS-induced ALI were studied compared with DIP injection. The results showed DIP liposomes have the relative high entrapment efficiency and satisfying particle size. Compared with DIP injection, the liposomes increased the accumulation of DIP in the lung on a vast scale. Furthermore, DIP liposomes alleviated the ALI induced by LPS significantly. All of the results suggested that DIP liposomes have the potential efficacy in treating ALI/ARDS due to their obvious lung targeting.  相似文献   

16.
药物保护肺毛细血管内皮细胞 降低SARS发病率   总被引:2,自引:0,他引:2  
戴德哉 《药学进展》2003,27(6):321-326
急性呼吸窘迫综合征(ARDS)的致病因素很多,但最终均形成急性肺损伤(ALI),主要由肺毛细血管内皮细胞损害所介导,虽采用医疗措施,包括吸氧及气管插管进行呼吸机呼吸等,病人死亡率仍高。传染性非典型肺炎(SARS)引起ALI时,出现肺动脉高压及肺纤维化,最终临床出现ARDS。ARDS的病理核心是肺毛细血管内皮细胞的损害,血管内皮细胞可作为治疗ARDS及SARS的靶点。SARS病毒感染后,引起细胞因子的释放,其中包括内皮素-1(ET-1),ET-1可强烈收缩血管及致炎症反应。本文讨论在致病因子作用下,ET-1的增多与形成ARDS、败血症、休克的关系,致病机制包括ET-1诱导iNOS生成、使细胞膜Ca^2 内流增多、促使氧化应激而造成ALI。ET-1致肺损伤主要由于激活ETB受体,而ALI时肺内纤维化,ET-1亦起着重要的作用。过多的ET-1可使ARDS病人形成肺动脉高压,以ET-1及其所参与的SARS及ARDS发病的各个环节为靶点,应用抗病毒药、抑制炎症的糖皮质激素及阻断冠状病毒侵入细胞的大分子药物,使用内皮素受体拮抗剂和多离子通道阻断剂CPU86017,可阻断感染冠状病毒后形成肺损伤、肺纤维化、肺动脉痉挛及肺动脉高压等,有可能明显降低SARS及ARDS的发病率及致死率。  相似文献   

17.
Despite recent advances in supportive care, acute lung injury (ALI) and its more severe form acute respiratory distress syndrome (ARDS) are clinical entities with high morbidity and high mortality. In systemic inflammation, like sepsis, uncontrolled host defense can lead to systemic activation of coagulation on the one hand, and attenuation of fibrinolysis on the other. In ALI/ARDS similar but local disturbances in fibrin turnover occur, leading to excessive alveolar fibrin deposition compromising pulmonary integrity and function. Therapies in patients with sepsis have specifically focused on coagulation disturbances. Evidence from preclinical and clinical investigations suggests pharmacologically targeting pulmonary "coagulopathy" could be of benefit to patients with ALI/ARDS as well. Recent animal studies have demonstrated that administration of heparins, activated protein C (APC), Antithrombin (AT), Tissue factor-Factor VIIa (TF-FVIIa) pathway inhibitors, plasminogen activators (PA) and thrombomodulin (TM) can attenuate pulmonary coagulopathy and reduce lung injury and/or improve oxygenation. Some of these studies have also shown anti-inflammatory effects of treatment targeting at coagulation. To date there are no published studies that have specifically studied the effects of anticoagulants on ALI/ARDS however there are on-going clinical trials. A solid base has to be provided by preclinical studies to justify clinical studies on new pharmacologic therapies for ALI/ARDS. In this systematic literature review we give an overview of the models for ALI/ARDS that have been used so far on the topic of pulmonary coagulopathy and focus on the pharmacological interventions that have been evaluated with these models. Finally, the applicability of the different approaches for future research on this subject will be discussed.  相似文献   

18.
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are associated with high mortality rates despite therapeutic advances. The pathogenesis of ALI and ARDS is similar to that of sepsis, as these disease states involve uncontrolled host defense responses that lead to inflammation, endothelial damage, enhanced coagulation, diminished fibrinolysis, and fibroproliferation. Recent studies of anticoagulants have shown positive outcomes in patients with severe sepsis. In addition, emerging evidence suggests that the use of anticoagulants, such as tissue factor pathway inhibitor, antithrombin, thrombomodulin, heparin, activated protein C, and fibrinolytics (plasminogen activators and particularly tissue plasminogen activator), may be useful in the treatment of ALI and ARDS. Data from experimental models of sepsis, ALI, and ARDS indicate that some of these agents improve lung function and oxygenation. Although clinical data are less convincing than these findings, results from clinical trials may influence the design of future studies.  相似文献   

19.
20.
Background: Sepsis and acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) are life-threatening syndromes characterised by inflammation and increased vascular permeability. Amongst other factors, the angiopoietin–tyrosine kinase with immunoglobulin-like and EGF-like domains 2 (Tie2) system is involved. Objective: To explore whether the angiopoietin–Tie2 system provides suitable targets for the treatment of sepsis and ALI/ARDS. Methods: Original experimental and patient studies on angiopoietins and sepsis/endotoxemia, inflammation, lung injury, hyperpermeability, apoptosis, organ functions and vital outcomes were reviewed. Results/conclusion: The angiopoietin–Tie2 system controls the responsiveness of the endothelium to inflammatory, hyperpermeability, apoptosis and vasoreactive stimuli. Angiopoietin-2 provokes inflammation and vascular hyperpermeability, while angiopoietin-1 has a protective effect. Targeted angiopoietin-2 inhibition with RNA aptamers or blocking antibodies is a potential anti-inflammatory and anti-vascular hyperpermeability strategy in the treatment of sepsis and ALI/ARDS.  相似文献   

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