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.     

COPD气道重塑相关机制的研究进展

慢性阻塞性肺疾病(Chronic Obstructive Pulmonary Disease,COPD)是一种可以预防、可以治疗的疾病,以不完全可逆的气流受限为特征,气流受限呈进行性加重,与肺部对有害气体或颗粒的异常炎症反应有关.气道重塑是COPD主要病理特点之一,COPD的气道重塑主要发生在小气道(内径＜2mm),早期有上皮细胞增生,黏液腺增生,亦有上皮鳞状细胞化生,纤毛上皮细胞异常.随着病变发展,逐渐出现杯状细胞增多,管腔黏液分泌增加,小气道管壁结缔组织成分沉积,管壁平滑肌增厚,气道壁血管增生,并最终形成纤维化和闭塞[1],出现显著的小气道阻力增高和气流受限.目前多数观点认为,COPD的气道重塑与气道炎症过程相伴随[2],但其具体机制尚未明确.本文就COPD气道重塑相关机制的研究进展作一综述,旨在进一步明确气道炎症与气道重塑之间的关系:是互为因果,还是相互独立.为COPD的抗炎、抗重构联合治疗提供依据.     

慢性阻塞性肺疾病与肺血管系统

COPD不仅累及气道,而且累及整个肺组织;不仅肺泡受到破坏,而且肺泡间隔组织中微血管、毛细血管前微动脉也受到损害。由于肺血管存在大量受体和血管活性物质,当肺血管内皮细胞等受到激活、损伤后,可发生功能紊乱,大量释放炎症介质,加重气道炎症;血管收缩和舒张障碍;内皮细胞和平滑肌细胞异常增生;肺血管重塑;低氧性肺动脉高压形成等。故近年认为肺血管系统在COPD的发病机制中的作用十分重要。甚至有学者提出将来的治疗策略应重视COPD的血管系统[1]。本文就其有关研究进展作一综述。1肺血管系统改变贯穿于COPD全程1.1吸烟与肺血管改变…     

慢性阻塞性肺疾病与肺癌的同源性表现及关联发病机制

COPD是累及中央气道、外周气道、肺实质和肺血管的复杂慢性全身炎症性疾病,肺癌是COPD的常见合并症之一,二者均与肺部对香烟烟雾等有害气体或颗粒的异常炎症反应有关,且COPD患者发生肺癌的风险增加[1],提示二者的发生过程存在相关性.为探讨这种相关性是否与烟雾暴露、遗传易感因素和(或)异常的免疫炎症反应有关,现将COPD和肺癌的流行病学、影响因素及发病机制等方面的生物学特征综述如下.     

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…     

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。     

哮喘、慢性阻塞性肺疾病和哮喘-慢性阻塞性肺疾病重叠综合征

哮喘和慢性阻塞性肺疾病(COPD)是最常见的阻塞性气道疾病.理论上,COPD和哮喘是不同的疾病,有着不同的自然病史和病理生理学基础.哮喘被认为是变态反应性疾病,常于儿童期起病,间断发作,气流阻塞完全可逆,气道高反应性,对抗炎治疗反应良好.而COPD与吸烟密切相关,中老年起病,慢性进展,固定的气道阻塞,不完全可逆的气流受限,伴随肺气肿、肺弹性回缩力的丧失以及肺弥散功能的异常.但在临床实践中,有时区分哮喘和COPD并非易事,部分患者同时具有哮喘和COPD的特点,即哮喘和COPD并存[1],称之为哮喘-COPD重叠综合征(简称重叠综合征)[2].下面结合国内外关于哮喘、COPD以及重叠综合征的最新研究进展,就其定义、流行病学、危险因素、炎症特征、气道重塑等方面对其进行阐述.     

慢性阻塞性肺疾病气道炎症与肺血管炎症相关性研究进展

慢性阻塞性肺疾病（COPD）气道炎症是重要的病理基础,它不仅是气道重构的开始而且对肺血管炎症与重构有重要影响。长期以来强调低氧因素在肺血管炎症中的作用,现发现无缺氧的轻度COPD患者甚至肺功能正常的吸烟者肺血管和外周气道均出现了炎症和重构。在COPD早期肺血管炎症与外周气道炎症是否就已同时启动？它们之间有何联系？本文收集近年来国内外研究,就COPD气道炎症与肺血管炎症的相关性作一简要综述。     

慢性阻塞性肺疾病与肺血管系统

COPD不仅累及气道，而且累及整个肺组织；不仅肺泡受到破坏，而且肺泡间隔组织中微血管、毛细血管前微动脉也受到损害。由于肺血管存在大量受体和血管活性物质，当肺血管内皮细胞等受到激活、损伤后，可发生功能紊乱，大量释放炎症介质，加重气道炎症；血管收缩和舒张障碍；内皮细胞和平滑肌细胞异常增生；肺血管重塑；低氧性肺动脉高压形成等。故近年认为肺血管系统在COPD的发病机制中的作用十分重要。甚至有学提出将来的治疗策略应重视COPD的血管系统。本就其有关研究进展作一综述。     

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.     

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…     

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.     

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.     

Ruptured pulmonary artery aneurysm mimicking pulmonary embolism

Aneurysms of the pulmonary artery are very rare pathological vascular conditions. Peripheral pulmonary aneurysms have been reported only in a few cases. The causes of these aneurysms include extensive degenerative changes, traumas, infection and congenital malformations. Because of the imminent danger of rupture, surgical treatment should always be preferred. The following case report demonstrates one of a multitude of possible misdiagnoses for rupture of a pulmonary aneurysm.     

Cavitating pulmonary infarcts revealing thromboembolic pulmonary hypertension

Several etiologies are involved in the pathogenesis of cavitating pulmonary disease including neoplastic, infectious or inflammatory processes. Another is pulmonary infarction associated with venous thromboembolism. The lung cavities tend to be located peripherally and are the result of pulmonary embolism. We report the case of a woman with chronic thromboembolic pulmonary hypertension (CTEPH), associated with familial thrombophilia, revealed by cavitating pulmonary infarcts. CTEPH is sometimes diagnosed during an episode of recurrent pulmonary embolism following previously unnoticed lesions. Thrombophilias such as isolated elevated factor VIII are risk factors for CTEPH.     

Balloon-occlusion pulmonary cineangiography for diagnosing pulmonary embolism

For the angiographic diagnosis of pulmonary embolism (PE) we performed balloon-occlusion pulmonary cineangiography in ten consecutive patients. The technical aspects of the balloon-occlusion cineangiographic technique are reviewed, and its complementary role in the diagnosis of PE are outlined and illustrated with several examples.