老年慢性阻塞性肺疾病患者血浆内皮素－1含量与PaO_2、PaCO_2及肺动脉压的关系

目的探讨血浆内皮素－１（ｅｎｄｏｔｈｅｌｉｎ－１，ＥＴ－１）在慢性阻塞性肺疾病（ｃｈｒｏｎｉｃｏｂｓｔｒｕｃｔｉｖｅｐｕｌｍｏｎａｒｙｄｉｓｅａｓｅ，ＣＯＰＤ）中的作用。方法应用放射免疫法测定４３例老年ＣＯＰＤ急性发作期患者和１５名健康对照者血浆ＥＴ－１水平，其中８例肺心病患者行右心微导管检测肺动脉压。结果ＣＯＰＤ患者和肺心病患者的血浆ＥＴ－１含量分别为５．２４±０．５０、５．８０±０．６６ｐｇ／ｍｌ，较健康对照组血浆ＥＴ－１含量（４．６５±０．６５ｐｇ／ｍｌ）明显升高（Ｐ值＜０．０１及０．００１）；血浆ＥＴ－１含量与ＰａＯ２呈显著性负相关（ＣＯＰＤ组：ｒ值＝－０．５８３，Ｐ值＜０．０１；肺心病组：ｒ值＝－０．６２７，Ｐ值＜０．００１），与ＰａＣＯ２呈显著性正相关（ＣＯＰＤ组：ｒ值＝－０．５１４，Ｐ值＜０．０５；肺心病组：ｒ值＝０．５９３，Ｐ值＜０．００１）；ＥＴ－１含量与肺动脉收缩压及平均压均存在正相关（ｒ值＝０．７２７及０．６８１，Ｐ值均＜０．０５）。结论血浆ＥＴ－１参与肺心病肺动脉高压的形成，缺氧和二氧化碳潴留是刺激ＥＴ－１释放的重要原因之一     

老年慢性阻塞性肺疾病患者血浆内皮素—1含量与PaO2,PaCO2…

探讨血浆内皮素－１在慢性阻塞性肺疾病中的作用。应用放射免疫法测定４３例老年ＣＯＰＤ急性发作期患者和１５名健康对照者血浆ＥＴ－１水平，其中８例肺心病患者行右心微导管检测肺动脉压。ＣＯＰＤ患者和肺心病患者的血浆ＥＴ－１含量分别为５．２４±０．５０、５．８０±０．６６ｐｇ／ｍｌ，较健康对照组血浆ＥＴ－１含量明显升高（Ｐ值〈０．０１及０．００１），血浆ＥＴ－１含量与ＰａＯ２呈显著性负相关组，ｒ值＝－０．５     

慢性阻塞性肺疾病和肺心病患者血液动力学与循环内皮细胞变化

目的探讨慢性阻塞性肺疾病（ＣＯＰＤ）和肺心病时血循环内皮细胞、血液动力学的变化及意义。方法运用右心导管检查技术和血循环内皮细胞（ＣＥＣ）分离技术，用硫巴比妥法及羟胺法测定血丙二醛（ＭＤＡ）及超氧化物岐化酶（ＳＯＤ）。结果肺心病组肺动脉平均压［（ｍＰＡＰ）３７６±０７５ｋＰａ、血ＣＥＣ数量每０９微升为１６７０±２６５与ＣＯＰＤ组（８４８±２２３）比较，差异有显著性（Ｐ＜０．０１），血ＣＥＣ数量与动脉血氧分压（ＰａＯ２）比较呈显著负相关（ｒ＝０．９４２３，Ｐ＜０．００１），血ＣＥＣ数量与肺动脉压比较呈显著正相关（ｒ＝０．８２７０，Ｐ＜０．００１），肺心病组丙二醛（ＭＤＡ）、超氧化物歧化酶（ＳＯＤ）与ＣＯＰＤ组比较，差异有显著性（Ｐ＜０．０１）。结论缺氧可加重血管内皮细胞损伤     

先天性心脏病伴肺动脉高压患者血浆心钠素水平

本文采用放射性免疫分析法测定３１例先天性心脏病患者血浆心钠素水平。结果表明，先天性心脏病伴肺动脉高压患者组（２１例）血浆心钠素水平明显高于无肺动脉高压组（１０例）（Ｐ＜０．０１）及正常对照组（Ｐ＜０．０１）；血浆心钠素水平随平均肺动脉压的升高而升高（ｒ＝０．７４，Ｐ＜０．００１），术后随肺动脉压的下降而降低。结果提示，血浆心钠素水平的升高在肺动脉高压的调节中可能起着重要作用。     

高血压患者血浆和淋巴细胞中血管紧张素Ⅱ、内皮素和一氧化氮的变化及关系

分析一组高血压病患者血浆和淋巴细胞中血管紧张素Ⅱ（ＡｎｇⅡ）、内皮素（ＥＴ）和一氧化氮（ＮＯ）含量的变化及它们间的相互关系。方法高血压（ＥＨ）组３９例，正常对照（ＮＣ）组４１例，放射免疫分析法测定ＡｎｇⅡ、ＥＴ，高效液相色谱分析法测定ＮＯ。结果ＥＨ患者血浆和淋巴细胞中ＥＴ均高于ＮＣ组（Ｐ分别＜０．０５和＜０．０１），ＮＯ低于ＮＣ组（Ｐ分别＜０．０５和＜０．０１）。除血浆ＥＴ和ＮＯ外，各指标改变ＥＨⅡ期较Ⅰ期明显（Ｐ分别＜０．０５和＜０．０１）。逐步回归分析表明，ＥＨ组平均动脉压（ＭＡＰ）与血浆及淋巴细胞中ＡｎｇⅡ、ＥＴ呈正相关，与ＮＯ负相关（ｒ分别＝０．６７，０．８１，Ｐ均＜０．０１）；ＥＨ组血浆和淋巴细胞中ＮＯ与ＡｎｇⅡ、ＥＴ均呈负相关（ｒ分别＝－０．６５１，－０．７２５，Ｐ均＜０．０１）。结论淋巴细胞反映血管内皮细胞内分泌功能比血浆更为敏感，与ＭＡＰ相关性更好，ＡｎｇⅡ、ＥＴ和ＮＯ三者分泌失平衡，是ＥＨ发病的重要原因之一。     

心功能障碍患者心肌组织及血浆肾素－血管紧张素系统、心钠素改变的临床意义

１９例心功能障碍患者的血浆、心肌血管紧张素Ⅱ（ＡｎｇⅡ）、心钠素（ＡＮＦ）含量高于正常对照组；血浆ＡｎｇⅡ和ＡＮＦ含量增高与心脏指数（ＣＩ）呈显著负相关（ｒ＝－０．５９６８，Ｐ＜０．０５；ｒ＝－０．８９９６，Ｐ＜０．０１），心肌ＡｎｇⅡ含量变化与左室心肌重量（ＬＶＭ）呈显著正相关（ｒ＝０．５７２３，Ｐ＜０．０５）；提示心脏局部肾素－血管紧张素系统（ＲＡＳ）活性增高和ＡＮＦ变化参与心肌细胞增殖及心室重塑的意义较为突出。     

老年脑出血患者血浆ET和ANP的变化及临床意义

目的测定老年脑出血患者血浆内皮素（ＥＴ）、心钠素（ＡＮＰ）浓度并探讨其临床意义。方法以放射免疫法测定老年和非老年健康人；老年及非老年脑出血患者不同时期血浆ＥＴ及ＡＮＰ水平。结果老年脑出血患者急性期血浆ＥＴ为１４８．１８ｎｇ／Ｌ，ＡＮＰ为５７．３３ｎｇ／Ｌ，较健康对照组明显升高（分别为Ｐ＜０．０１及Ｐ＜０．０５）。恢复期与对照组比较无明显差异。同期测定的非老年脑出血患者血浆ＥＴ和ＡＮＰ浓度与老年患者差异无显著意义（Ｐ＞０．０５），直线相关分析表明，老年脑出血患者急性期血浆ＥＴ与ＡＮＰ之间呈明显正相关。结论脑出血患者血浆ＥＴ、ＡＮＰ浓度的升高与脑出血的发生、病情的发展及转归有密切关系     

肝硬化门脉高压患者的肺动脉血流动力学研究

应用多普勒超声心动图（ＤＥＣ）对３２例肝硬化门脉高压（ＣＨＰ）患者的肺动脉血流动力学（ＰＡＨ）进行了系统检测。结果：患者组比正常对照组肺动脉增宽（Ｐ＜０．００５），血流速度变慢（Ｐ＜０．００５），血流量增加（Ｐ＜０．０５），心脏指数增大（Ｐ＜０．０５），压力阶差缩小（Ｐ＜０．０５）。提示ＣＨＰ患者的肺血管处于扩张状态，ＰＡＨ呈高动力循环状态，肺动脉扩张和高动力循环状态是肝－肺综合征的病理基础。     

氧疗及正压通气对慢性阻塞性肺病患者夜间低氧血症的疗效

为了观察夜间氧疗及加用持续正压通气对急性加重期慢性阻塞性肺病（ＣＯＰＤ）患者夜间低氧血症的治疗效果，用脉搏氧饱和度仪对５８例患者进行监测描记，并作动脉血气分析。结果表明，白天动脉血氧分压（ＰａＯ２）、动脉血二氧化碳分压（ＰａＣＯ２）及基础脉搏氧饱和度（ＳｐＯ２）与夜间平均脉搏氧饱和度（ＭＳｐＯ２）之间有显著的正相关（ｒ＝０．７０２，ｒ＝０．６１３，ｒ＝０．６０５，Ｐ值均＜０．０１），与夜间呼吸空气时比较，３７例患者夜间氧疗效果良好，夜间平均ＳｐＯ２、平均最低ＳｐＯ２（ｍＳｐＯ２）升高（Ｐ＜０．０１），氧降累计时间百分比（ＣＴＮＯＤ％）降低（Ｐ＜０．０１）。其余２１例患者疗效不佳，改用夜间氧疗加持续正压通气（ＢｉＰＡＰ）后效果极好，夜间ＭＳｐＯ２、ｍＳｐＯ２与ＣＴＮＯＤ％三项指标均显著改善（Ｐ＜０．０１），且睡后ＰａＯ２升高（Ｐ＜０．０１），ＰａＣＯ２降低（Ｐ＜０．０１）。证实夜间氧疗能纠正多数ＣＯＰＤ患者的夜间低氧血症，对疗效不良者加用无创持续正压通气可获满意效果。     

肺心病患者血浆内皮素含量变化观察分析

采用放射免疫分析法测定２８例肺心病患者及１４例正常人血浆内皮素（ＥＴ）含量，并同时作动脉血气分析及测定部分患者肺血管阻力（ＰＶＲ）、心输出量（ＣＯ）。结果：肺心病组血浆ＥＴ明显高于正常人（Ｐ＜０．０１），急性期显著高于缓解期（Ｐ＜０．０１）。血浆ＥＴ与ｐＨ、ＰａＯ２呈显著负相关（Ｐ＜０．０１），与ＰＶＲ呈显著正相关（Ｐ＜０．０１），与ＣＯ是显著负相关（Ｐ＜０．０１）。提示；低氧血症和酸血症可能是刺激血浆ＥＴ升高、引起肺血管内皮功能紊乱的重要因素；ＥＴ在肺血管阻力增加、肺动脉高压形成的病理过程中有其重要的作用。     

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.