血清胎盘生长因子在慢性阻塞性肺疾病中的作用

慢性阻塞性肺疾病(COPD)的发展过程中可逐渐发生肺动脉高压.肺血管重构是肺动脉高压的主要原因,肺血管重构与COPD的发展密切相关[1],有许多炎症介质、细胞因子的参与.已有研究证实血管内皮生长因子(VEGF)及其受体(VEGFR)与COPD气道壁重塑、上皮细胞和内皮细胞的凋亡、肺血管重塑有关系.而胎盘生长因子(PIGF)作为VEGF家族的一员,在诱导血管生成和维持血管的正常结构和功能中有着重要作用.本研究通过测定不同程度COPD的PIGF水平变化,分析其与VEGF、肺功能、肺动脉收缩压(PSAP)、动脉血氧分压的(PaO2)相关性.     

炎症在慢性阻塞性肺疾病相关肺动脉高压发病机制中的作用的研究进展

慢性阻塞性肺疾病(COPD)是以气道、肺实质、肺血管慢性炎症为主要特征的慢性肺疾病.肺动脉高压是COPD的主要并发症.近年来新的研究表明,COPD相关肺动脉高压的主要发病机制除缺氧外,炎症介质如白介素16、C反应蛋白、肿瘤坏死因子α、内皮素1等及炎症细胞如中性粒细胞、T淋巴细胞、巨噬细胞、肥大细胞等也起重要作用.     

血管内皮生长因子与慢性阻塞性肺疾病继发肺动脉高压的关系

血管内皮生长因子(vascular endothelial growth factor,VEGF)是一种重要的血管内皮细胞丝裂原和通透因子.肺血管的重塑与慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)继发肺动脉高压密切相关.VEGF贯穿于COPD发展的全过程,在COPD的不同时期呈现不同的表达水平,发挥不同的生物学作用.气道炎症、低氧等因素可以在COPD早期促进VEGF及其受体的表达上调从而导致肺血管重塑的发生发展,VEGF也可以对COPD后期继发肺动脉高压时的重度肺血管重塑起到一定的修复作用.通过阐述VEGF、COPD肺血管重塑及继发肺动脉高压之间的相互关系,可以对COPD继发肺动脉高压的诊断和治疗提供新的思路.     

慢性阻塞性肺疾病患者系统性炎症与肺动脉高压的关系研究

目的探讨慢性阻塞性肺疾病(COPD)伴或不伴肺动脉高压与全身炎症反应的程度的关系。方法采用彩色多普勒超声心动图测定安静状态下收缩期肺动脉压(SPAP),并将46例COPD患者分为肺动脉高压组和无肺动脉高压组,测定患者血循环中的C反应蛋白(CRP)、肿瘤坏死因子α(TNF-α)以评估COPD全身炎症反应的程度。结果 46例患者,其中21例并发肺动脉高压,25例无肺动脉高压。肺动脉高压组患者血清CRP中位数17.5mg/L及TNF-α中位数7.4pg/ml,显著高于无肺动脉高压组患者的血清CRP中位数11.8mg/L及TNF-α中位数5.1pg/ml,差异均有统计学意义(P0.05)。CRP对数转换值与SPAP呈正相关(r=0.637,P0.05)。TNF-α对数转换值与SPAP无相关性。结论系统性炎症与COPD肺动脉高压形成有关。     

慢性阻塞性肺疾病肺血管炎症的研究进展

COPD是累及气道、肺实质和肺血管的慢性炎症,气道炎症在COPD的发展中起着重要作用,但目前对于肺血管炎症(尤其是小动脉炎症)的研究及关注较少.有研究结果 表明,肺功能正常的长期吸烟者以及未发生缺氧的轻度COPD患者已经存在肺血管明显的炎症反应[1],并出现肺血管内皮结构异常和肺血管重塑[2],吸烟和肺血管炎症可能是COPD肺血管重塑的始动因素.为此,我们对COPD肺血管炎症的特征、相关因素和机制的研究进展进行综述.     

慢性阻塞性肺病相关肺动脉高压与炎症反应

<正>2013年GOLD将慢性阻塞性肺病(COPD)定义为是一种以持续气流受限为特征的可以预防和治疗的疾病。其气流受限多呈进行性发展,与气道和肺组织对烟草烟雾等有害气体或有害颗粒的慢性炎性反应增强有关[1]。COPD患者肺实质及肺血管均存在炎症反应[2]。大约有20%的COPD患者可进展为肺动脉高压[3],COPD继发肺动脉高压的机制尚不是很清楚,一直以来认为慢性缺氧所致的肺血管     

支气管哮喘和慢性阻塞性肺疾病气道重塑的差异

支气管哮喘(以下简称“哮喘”)和慢性阻塞性肺疾病(COPD)均为气道炎症性疾病,尽管其发病机制不同,但气道炎症均可导致气道壁的增厚和肺实质结构的改变,从而引起气道的狭窄和气流的受限。这样一个以气道壁增厚和炎症存在为特点的气道重塑的过程在哮喘和COPD中已有报道,但气道炎症细胞的浸润和重塑在这两种疾病中有所不同[1]。本文主要阐述哮喘和COPD气道重塑的主要差异,以便更好地了解气道重塑的机制,寻求新的治疗这些疾病的目标。1气道炎症及其与重塑的关系哮喘和COPD气道炎症的病理变化过程既存在于中央气道,也存在于外周气道,这个…     

慢性阻塞性肺疾病并发肺动脉高压与炎症反应的相关性研究

目的:通过对C反应蛋白(CRP)、白介素(IL-6)、肿瘤坏死因子(TNF-α)及B型脑尿钠肽(BNP)的检测,观察炎症反应与慢性阻塞性肺疾病(COPD)并发肺动脉高压的关系。方法:收集首都医科大学附属北京安贞医院呼吸科及急诊重症监护病房,2011年9月至2012年7月收治的COPD患者80例,其中女性32例,男性48例;平均年龄(74±9)岁;平均FEV1%预计值为(59.4±29.4)%;根据彩色多普勒超声心动仪测定肺动脉收缩压;颗粒增强免疫透射比浊法(PETIA)测定血清CRP,酶联免疫吸附法(ELISA)测定血清IL-6及TNF-α,化学发光微粒子免疫检测法(CMIA)测定血浆BNP。结果:80例患者中COPD并发肺动脉高压组(A组)及COPD肺动脉压正常组(B组)各40例。A组CRP[中位数6.5(2.7～21.1)mg/L]、IL-6[中位数106.6(41.0-368.6)ng/L]、TNF-α[(19.4±10.2)ng/L]、BNP[中位数137.0(92.2～299.6)ng/L],均高于B组患者:CRP[中位数1.9(0.6～5.2)ng/L]、IL-6[中位数73.9(12.0～152.1)ng/L、TNF-α[(14.9±5.3)ng/L]、BNP[中位数45.1(20.4-98.5)ng/L]。各因子水平存在显著差异,且差异具有统计学意义(P<0.05)。Logistic回归分析提示CRP、BNP与COPD并发肺动脉高压相关。结论:COPD并发肺动脉高压患者CRP、IL-6、TNF-α及BNP较COPD肺动脉压正常患者高,提示炎症反应可能是COPD患者形成肺动脉高压的重要因素。     

C反应蛋白和内皮素-1在慢性阻塞性肺疾病合并肺动脉高压患者中的表达

肺动脉高压是COPD的常见并发症,可导致COPD的临床过程逐渐恶化,增加COPD患者的住院风险[1].已有研究结果表明,慢性炎症和肺血管结构重塑有关[2],C反应蛋白和内皮素-1与肺动脉高压有关[3-4].本研究旨在探讨COPD合并肺动脉高压患者血浆中C反应蛋白和内皮素-1的水平,以及C反应蛋白和内皮素-1之间的关系.     

慢性阻塞性肺疾病中炎症细胞、细胞因子与肺功能的关系

慢性阻塞性肺疾病(COPD)是一种由不同的炎性细胞、细胞因子和炎性介质介导的慢性气道炎症性疾病。炎症所涉及的部位包括呼吸道、肺血管及肺实质,气道炎症的持续存在、肺组织结构的破坏、气道的重塑、肺功能的下降都与炎性介质有关。本文就炎症反应与COPD肺功能关系作一综述,揭示炎症反应对COPD患者肺功能的影响。     

肺动脉血栓内膜剥脱术后再灌注肺水肿的进展

肺血栓栓塞症是一种常见、多发且病死率和致残率高的疾病。大多数急性肺动脉血栓栓塞经及时的溶栓抗凝等治疗和 (或 )自身的纤溶系统能将血栓不同程度地溶解 ,另有0 1%～ 0 2 %的患者因血栓在急性期未能溶解或栓塞反复发生进而发展成慢性栓塞性肺动脉高压。慢性栓塞性肺动脉高压溶栓无效 ,抗凝、扩血管治疗效果不佳 ,其病理过程多呈进行性加重或稳定一段时间后再次加重 ,自然预后差。肺动脉平均压 >3 0ｍｍＨｇ(1ｍｍＨｇ =0 13 3ｋＰａ)的慢性栓塞性肺动脉高压患者 5年生存率为 3 0 % ,肺动脉平均压 >5 0ｍｍＨｇ者仅为 10 %。肺动脉血…     

Chronic pulmonary embolism and pulmonary hypertension

Incomplete resolution of acute pulmonary embolism (PE) is frequently observed after acute PE and may rarely result in chronic thromboembolic pulmonary hypertension (CTEPH). The underlying pathophysiological mechanism is largely unknown. Evidence underlines the concept of a dual pulmonary vascular compartment model consisting of increased pulmonary vascular resistance by both large vessel obstruction and distal small vessel obliteration, the latter initiated by pathological vascular remodeling. Up to 40% of patients with established CTEPH have no prior history of symptomatic venous thromboembolism. CTEPH is associated with a poor prognosis if left untreated. Therefore, the diagnostic approach of CTEPH aims at assessing the location and extent of the embolic obstruction, establishing the operability and prognosis of the patients and ruling out other variations of pulmonary hypertension with distinct indicated treatment. Heart catheterization for invasive pressure measurements and pulmonary catheter angiography is obligatory for the final diagnosis. Pulmonary thromboendarterectomy is the treatment of choice. In certain patients with persistent or recurrent pulmonary hypertension after surgery or with inoperable disease, pharmacotherapy might be beneficial.     

Retrograde pulmonary perfusion improves results in pulmonary embolectomy for massive pulmonary embolism

Mortality rates for pulmonary embolectomy in patients with acute massive pulmonary embolism have decreased in recent years. However, they still range from 30% to 45% when the surgery is performed on critically ill patients, and the rates reach 60% in patients who have experienced cardiac arrest before the procedure. The causes of death in these patients are generally attributed to right heart failure due to persistent pulmonary hypertension, intractable pulmonary edema, and massive parenchymal and intrabronchial hemorrhage. Clinical and experimental findings indicate that venous air embolism causes severe or even lethal damage to the pulmonary microvasculature and the lung parenchyma consequent to the release of endothelium-derived cytokines. These findings are similar to those observed when severely compromised patients undergo pulmonary embolectomy-air entrapped in the pulmonary artery during embolectomy can lead to fatal outcomes.Besides enabling the removal of residual thrombotic material from the peripheral branches of the pulmonary artery, retrograde pulmonary perfusion fills the pulmonary artery with blood and prevents pulmonary air embolism. In this retrospective study, we analyzed a series of 21 consecutive critically ill patients in whom we applied retrograde pulmonary perfusion while performing standard pulmonary embolectomy. No patient died or experienced major postoperative complications. We believe that the use of retrograde pulmonary perfusion decreases morbidity and mortality rates associated with pulmonary embolectomy in critically ill patients.     

Residual pulmonary thromboemboli after acute pulmonary embolism

BackgroundAfter an acute pulmonary embolism (PE), the complete resolution of thromboemboli may not be routinely achieved. The rate of persistence may depend on the time and the diagnostic technique used for evaluation.Patients and methodsPatients were diagnosed with acute PE by means of computed tomography angiography (CTA). While they were receiving anticoagulant therapy, a second CTA was used to explore the rate of persistence of residual thromboemboli. During the initial episode, the plasma levels of Troponin I and natriuretic peptide, patient demographics, and hemodynamic and gas exchange data were evaluated as risk factors for persistence of pulmonary thromboemboli.ResultsIn this study 166 patients were diagnosed. A second CTA was not made in 46 (28%) patients for different reasons. In 120 (72%) patients a second CTA was made 4.5 [SD2.34] months after the initial episode (range 2–12 months). Complete clearance of thrombi occurred in 89 (74%, 95% CI 65–81) patients. Residual thrombi remained in 31 (26%, 95% CI 18–34) patients. In 6%, 13% and 81% of the patients the size of the residual thrombi was greater, similar to and smaller than initially diagnosed, respectively.The risk factors for residual thrombi included the thrombotic burden (OR 1.95), the alveolar to arterial difference of oxygen (OR 1.64), and the clinical antecedents of venous thromboembolic disease (OR 0.65).ConclusionsAfter 4.5 months of anticoagulant therapy, residual pulmonary thromboemboli persisted in 26% of the patients. The risk factors for residual thromboemboli include a greater initial thrombotic burden, a deeper gas exchange disturbation and a history of previous venous thromboembolism.     

Acute pulmonary embolism and pulmonary infarction]

32 cases of pulmonary embolism were reported, 18 cases had been autopsied (massive pulmonary embolism 9 cases. moderate pulmonary embolism 23 cases). The incidence risk factors pathogenesis, clinical manifestations of pulmonary embolism were presented. The relation between pulmonary embolism and pulmonary infarction and treatment of massive pulmonary infarction were discussed.     

Reperfusion pulmonary edema after pulmonary artery thromboendarterectomy

Pulmonary artery thromboendarterectomy (PAT) is a potentially curative procedure in chronic, major vessel thromboembolic pulmonary hypertension. However, postoperative reperfusion pulmonary edema (RPE) has been a serious complication, often requiring prolonged mechanical ventilation. This entity has been described only anecdotally in the past. To characterize it more fully, we retrospectively analyzed the course and potential determinants of RPE after thromboendarterectomy in 22 patients who had PAT at our institution from 1969 through 1984. Particular attention was directed to clinical data, thrombus location, areas operated, postoperative roentgenograms, and preoperative and postoperative hemodynamic data. In all patients but 1, RPE developed within 72 h after surgery, corresponding to anatomic locations distal to vessels subjected to PAT. Regions of lung not reperfused at surgery were uniformly spared. Pulmonary capillary wedge and/or left atrial pressures preoperatively and postoperatively were not elevated. None of the preoperative data predicted which patients would develop more persistent RPE. These observations suggest that the phenomenon of RPE is a peculiar, focal form of pulmonary edema, the basis for which remains to be defined.     

Nitroglycerin-responsive pulmonary hypertension in idiopathic pulmonary hemosiderosis

Idiopathic pulmonary hemosiderosis (IPH) is an uncommon disease found predominantly in pediatric patients. It can produce severe chronic pulmonary injury that results in chronic hypoxemia, pulmonary insufficiency, and progressive pulmonary fibrosis, leading to irreversible pulmonary hypertension and death. We studied the pulmonary hemodynamics in an 9-yr-old boy with IPH to determine if pulmonary hypertension contributed to exacerbations of this disease. Our results showed that this patient demonstrated pulmonary hypertension during acute exacerbations. Initially, the elevated pulmonary artery pressure responded both to oxygen and to a pulmonary vasodilator in the form of nitroglycerin. However, this improvement was not sustained. We conclude that pulmonary hypertension is probably a result of chronic hypoxemia experienced by patients with pulmonary hemosiderosis. Further investigation is warranted to assess whether or not intervention aimed at reducing pulmonary artery pressure in IPH improves outcome.     

Primary pulmonary artery sarcoma mimicking pulmonary thromboembolism

A 69-year-old woman presenting with dyspnea had a pericardial window created for fibrinous pericarditis. The patient subsequently developed pulmonary hypertension and a ventilation perfusion scan was compatible with pulmonary thromboembolism. A primary tumour of the pulmonary artery was suggested by angiography, computerized axial tomography and magnetic resonance imaging. Pathology confirmed a spindle cell pulmonary artery sarcoma.