幼兔胎粪吸入后肺表面活性蛋白B动态改变及与右心室压力关系的探讨

目的　探讨胎粪吸入综合征 (MAS)并发持续肺动脉高压 (PPHN)的发病机制。方法(1)通过气管内灌入胎粪 0 .6ml kg和 4ml kg建立轻、重度幼兔胎粪吸入模型 ;(2 )应用右心室穿刺法经压力传感器与日本光电公司生产的RM 6 0 0 0型多道生理记录仪相连 ,测定轻度胎粪吸入组 16、2 4、48、72h和重度胎粪吸入组右心室收缩压 ;(3)用RT PCR检测技术检测肺表面活性物质蛋白B(SP B)mRNA的水平。结果　 (1)轻度胎粪吸入组右心室收缩压从胎粪吸入后 16h开始升高 (19.3± 0 .8)mmHg(1mmHg=0 .133kPa) ,2 4h达高峰 (2 6 .8± 1.1)mmHg,72h恢复正常 (14.2± 0 .3)mmHg。重度胎粪吸入组右心室收缩压为 (32 .7± 1.1)mmHg ,明显高于轻度胎粪吸入组和对照组 (q值分别为17.5 6、5 5 .78,P均 <0 .0 1) ;(2 )轻度胎粪吸入组肺组织SP BmRNA吸光度 (A值 )较对照组降低 ,2 4～48h达最低水平 ,为 (0 .74± 0 .0 8) ,72h基本恢复正常 (1.84± 0 .10 ) ,重度胎粪吸入组SP BA值为(0 .2 0± 0 .0 5 ) ,较轻度胎粪吸入组降低更明显。SP BmRNA的A值与右心室压亦呈明显负相关 (r =- 0 .84,P <0 .0 1,n =30 )。结论　 (1)胎粪吸入后肺表面活性物质减少 ,并与胎粪吸入浓度有关 ,提示MAS时肺病理生理改变及其严重程度与其表面活性物质功能障碍有     

Changes of Fibrinolysis and Their Relationship with Pulmonary Artery Pressures in Neonates with Lung Diseases

目的　研究新生儿肺疾病的纤溶改变及其与肺动脉压力的关系。方法　用发色底物法测定 2 7例新生儿肺疾病患儿 (病例组 )及 2 5例正常新生儿 (对照组 )血浆组织纤溶酶原激活剂 (TPA)和纤溶酶原激活抑制物(PAI)活性变化 ;用超声多普勒方法测定肺动脉血流加速时间 (TPV)与右室射血时间 (RVET)之比值 (TPV/RVET) ,以此估计新生儿肺动脉压力 (TPV/RVET比值与肺动脉压力成反比 )。结果　病例组PAI活性 [(9.3±4 .1)AU× 10 -1/ml]明显高于对照组 [(5 .5± 3.0 )AU× 10 -1/ml],P <0 .0 1,TPV/RVET比值 (0 .2 9± 0 .0 5 )明显低于对照组 (0 .34± 0 .0 8) ,(P <0 .0 5 ) ;发生肺出血者肺动脉压力 [TPV/RVET (0 .2 3± 0 .0 2 ) ]显著升高 ,P <0 .0 5。肺出血恢复期新生儿TPA [(3.7± 1.7)IU× 10 -1/ml]及血小板 [(180± 30 )× 10 9/L]明显高于肺出血发生时 [TPA (1.8± 0 .7)IU× 10 -1/ml,血小板 (98± 39)× 10 9/L],(P <0 .0 1)。结论　新生儿肺疾病时由于肺动脉压力增高 ,肺血管内皮细胞破坏 ,导致TPA释放减少 ,PAI活性增高 ,纤溶活性降低。     

吸入一氧化氮治疗大鼠缺氧性肺动脉高压

目的　 观察吸入一氧化氮 (NO)对慢性和急性缺氧所致大鼠肺动脉高压的作用。 方法 　分别利用雄性Wistar大鼠 3 0只 ,制备慢性和急性缺氧肺动脉高压模型。实验中监测肺动脉压、血气、高铁血红蛋白含量 (Met % )等指标。 结果 　慢性缺氧大鼠吸入 2 0 ppm、40ppmNO ,肺动脉平均压 (MPAP)由治疗前 (2 5 2± 3 5 )mmHg降到 (2 2 4± 3 5 )mmHg及 (2 1 8± 3 3 )mmHg ,而对动物体循环血压无明显影响 ;急性缺氧大鼠吸入 2 0 ppm、40 ppmNO 1hMPAP分别由缺氧时 (2 2 8± 2 7)mmHg、(2 4± 2 8)mmHg下降到 (19 6± 4 7)mmHg和 (2 0 5± 4 1)mmHg。吸入NO 4h ,2 0ppm组Met %由 (0 40± 0 3 9) %升到 (0 95±0 75 ) % ,40 ppm组由 (0 3 9± 0 3 2 ) %升到 (1 2 6± 0 49) %。肺病理组织检查显示 :2 0 ppm、40 ppm组与对照组无显著差别。 结论 　吸入NO对慢性和急性缺氧肺动脉高压具有选择性扩张肺血管的作用 ,急性缺氧大鼠持续吸入NO 4h不会引起高铁血红蛋白血症 ,对肺组织结构无重要影响     

新生儿窒息肺动脉压力变化的无创性动态监测

目的　研究新生儿窒息后肺动脉压力的变化特点及临床意义 ,提供简便无创的检测方法。方法　应用彩色脉冲多谱勒超声于生后 2 4h内、3、7及 12～ 14d分别检测了 30例窒息新生儿及 2 5例正常新生儿左 /右心室射血前期、左 /右心室射血时间及其比值的变化 ,并依此推算肺动脉压力。结果　窒息与正常新生儿肺动脉压力在 2 4h内分别为肺动脉舒张压 (5 5 1± 17 3)mmHg对 (15 0± 3 0 )mmHg ,肺动脉阻力 (14 2± 3 9)mmHg/(L·min·m2 )对 (5 3± 1 3)mmHg/(L·min·m2 ) ,肺循环阻力 /体循环阻力比值 (0 84± 0 4 7)对 (0 2 7± 0 2 0 ) ,差异极显著 ,P <0 0 1。至生后 1周末 ,两组婴儿上述各指标间均无明显差异。结论　肺动脉高压是新生儿窒息的重要病理生理变化 ,在生后 1周内应重视对窒息新生儿肺动脉压力的检测。多谱勒超声心动图简便、无创 ,适于观察新生儿肺动脉压力的变化     

高肺血流所致肺血管结构重建时内源性一氧化氮体系的研究

目的　探讨高肺血流所致肺血管结构重建时内源性一氧化氮 (NO)体系的变化。方法对大鼠行腹主动脉 下腔静脉分流术。 11周后以右心导管法测定肺动脉平均压 (mPAP) ,检测右心室 /左心室 +室间隔 [RV/(LV +S) ]的比值。观测肺血管显微及超微结构的变化 ,并且以分光光度计测定血浆NO含量 ,分别以原位杂交和免疫组织化学的方法检测肺动脉内皮型NO合酶 (eNOS)mRNA和蛋白的表达。结果　分流组大鼠mPAP明显高于对照组 [分别为 (2 2 5± 2 6)mmHg、(15 8± 2 8)mmHg,1mmHg =0 13 3kPa ,P <0 0 1],RV/(LV +S)比值也明显增加。光镜下 ,肺小血管肌化程度明显增强 ,肺中、小型肌型动脉相对中膜厚度明显增加。电镜下 ,肺腺泡内动脉内皮细胞增生、变性 ,内弹力层粗细不均 ,平滑肌细胞肥厚、向合成表型转化。并且分流组大鼠血浆NO含量明显高于对照组 [分别 (为3 0 2± 7 9) μmol/L、(19 7± 5 7) μmol/L ,P <0 0 1],肺动脉eNOSmRNA和蛋白表达均明显增强。 结论　NO体系 eNOSmRNA表达、eNOS蛋白表达及血浆NO含量上调在高肺血流所致肺动脉高压和肺血管结构重建的形成中起重要的调节作用     

先天性心脏病肺动脉高压肺组织超微结构的改变及临床意义

目的　探讨先心病肺动脉高压 (PH)患儿肺组织超微结构的改变及其临床意义。方法　 2 1例先心病患儿为 1997年 11月～ 1999年 2月间住院行心血管手术者 ,全组平均肺动脉压为 (5 8± 2 1)mmHg ,肺血管阻力 (760± 2 0 6)dyn·s·cm-5。除 4例动脉导管未闭 (PDA)行导管结扎外 ,其余患儿均在体外循环下行心内直视手术 ,于开胸后立即取肺组织在电镜下观察肺组织超微结构的变化。结果　 2 1例PH患儿肺组织均有不同程度的纤维化 ,且在毛细血管两侧不对称 ,主要集中于非气血交换侧 ,以胶原纤维增生最显著 ,弹力纤维增生次之。肺泡Ⅱ型细胞显著增多 ,其胞质内可见大量的线粒体、粗面内质网 ,板层小体增多并可见其内容物丢失。肺泡Ⅰ型细胞基膜显著增厚 ,肺小动脉平滑肌细胞增生 ,毛细血管基膜增厚。结论　重症先心病PH患儿肺组织超微结构发生明显改变 ,结合临床 ,提示对于先心病患儿宜尽早手术纠治 ,以从根本上消除形成PH的条件。     

高浓度氧对新生鼠肺血红素加氧酶-1蛋白表达的影响

目的　探讨高浓度氧对新生鼠肺损伤及肺血红素加氧酶 1(HO 1)蛋白表达的影响。方法　将生后 4～ 7d新生SD大鼠 5 7只随机分为 0、2 4、4 8、72h空气对照组和 2 4、4 8、72h高氧暴露组 ,分别置于空气中和常压高氧舱 (氧浓度 92 %～ 94 % )中 ,后断头处死后取肺组织 ,对肺组织切片在光镜、电镜下进行病理组织学观察 ,对肺组织湿 /干重比值进行比较 ,采用免疫组织化学分析对HO 1蛋白表达进行半定量及定位分析。结果　高氧组与空气对照组比较 ,肺组织有明显水肿、出血和炎症 ,电镜下观察病变主要在毛细血管内皮细胞 ;高氧 72h组肺组织湿 /干重比值 (7.97± 1.18)较 72h空气对照组 (6 .4 0± 0 .37)明显升高 (P <0 .0 5 ) ;高氧 72h组肺组织HO 1蛋白表达 (0 .5 0 4± 0 .0 6 2 )较 72h空气对照组 (0 .345± 0 .0 2 4 )明显升高 (P <0 .0 1) ;高氧暴露组HO 1蛋白呈强阳性表达 ,主要分布在支气管、肺泡上皮细胞和肺泡巨噬细胞。结论　高浓度氧可引起新生鼠肺损伤 ,且高浓度氧可引起新生鼠肺HO 1蛋白表达上调 ,证明HO 1参与新生鼠高氧肺损伤的病理生理过程     

一氧化氮吸入治疗新生儿肺动脉高压疗效的初步评价

利用彩色多普勒超声心动图技术 ,评价一氧化氮 (NO)吸入治疗新生儿肺动脉高压的疗效。对 8例新生儿因肺炎、肺透明膜病、持续胎儿循环和先天性支气管肺发育不良并发呼吸衰竭而采用机械通气和NO吸入治疗。NO吸入浓度为 3～2 0ppm ,吸入时间为 1小时～ 35天。多普勒超声心动图利用三尖瓣返流或动脉导管未闭定量估测NO吸入前后肺动脉收缩压 (SPAP) ,同时测量上肢收缩压 (SBP) ,计算肺 /体压力 (Pp/Ps)比值。结果显示 :NO吸入 30～ 1 2 0分钟和 1 8～ 2 4小时后 ,SPAP分别由NO吸入前的 5 7± 1 1 .6mmHg降至 41± 1 0 8mmHg和 43± 1 8 2mmHg ;Pp/Ps分别由 0 87± 0 1 5降至 0 6 1± 0 1 5和 0 6 3± 0 2 1。NO吸入前后SBP无明显变化。NO吸入后卵圆孔、动脉导管和室间隔缺损水平右向左或双向分流较吸入前明显减少。结论　NO吸入治疗新生儿肺动脉高压安全有效。彩色多普勒超声心动图技术对于指导NO的临床应用具有重要价值     

多普勒血流频谱法估测肺出血新生儿肺动脉压的研究

目的　研究肺出血新生儿心脏收缩功能和肺动脉压力变化及临床影响因素。方法　用M型二维超声多普勒和脉冲多普勒方法分别测定28例肺出血新生儿和28例非肺出血新生儿(含17例正常新生儿)心脏收缩功能及主肺动脉血流速度频谱,以肺动脉血流峰速时间/右室射血时间(TPV/RVET)比值反映肺动脉压力,分析肺出血新生儿心脏收缩功能和肺动脉压力变化及临床影响因素。结果　肺出血新生儿TPV/RVET比值(0.253±0.041)明显低于正常对照组(0.329±0.058)和非肺出血组(0.301±0.022)(P＜0.01);肺出血新生儿恢复期该比值(0.294±0.033)升高,肺出血死亡组TPV/RVET比值(0.219±0.022)和缩短分数［FS(31±5)%］明显低于存活新生儿(0.270±0.031,TPV/RVET39±7,FS)(P＜0.01);TPV(52±12)ms明显低于存活新生儿(44±8)(P＜0.05)。早产儿肺出血组TPV明显缩短(P＜0.01)。肺出血组TPV/RVET比值与动脉血pH值高度相关(r=0.84,P＜0.01)。结论　肺出血新生儿伴有肺动脉压力升高,严重者心脏收缩功能降低,导致心力衰竭,致新生儿死亡。     

肺表面活性制剂治疗新生儿呼吸窘迫综合征多中心临床观察

目的　评价肺表面活性制剂 (PS)在治疗新生儿呼吸窘迫综合征 (NRDS)的疗效和安全性。方法　对 4个医院的 42例NRDS患儿用curosurf (PS的一种 )治疗 ,观察治疗前后患儿肺功能和肺泡充气程度的变化及早产儿部分常见并发症的发生率。结果　用药后 30min患儿PaO2 和动脉 肺泡氧分压比值 (a/APO2 )明显上升 ,分别从 (44± 14)mmHg (1mmHg =0 .133kPa)上升至 (10 2± 5 9)mmHg和从 0 .11± 0 .0 5上升至 0 .2 8± 0 .18。用药后 1h、6h、12h、2 4h、3d和 10d的PaO2 和a/APO2 仍在较高水平 ,与用药前比较 ,差异均有非常显著意义 (P均 <0 .0 1)。用药后 30min ,患儿PaCO2 从用药前的 (5 4± 17)mmHg下降至 (45± 13)mmHg (P <0 .0 5 )。用药后 12h ,胸部X线片显示 ,患儿肺野透亮度明显改善 ,与用药前比较 ,差异有非常显著意义。用药后患儿颅内出血、气胸、动脉导管开放和肺炎等并发症的发生率分别为 2 8%、7%、35 %和 79%。结论　curosurf治疗能快速、安全、有效地改善NRDS患儿的肺功能和肺泡充气程度。     

High-altitude pulmonary edema with absent right pulmonary artery

High-altitude pulmonary edema potentially is fatal. Adults with unilateral absence of a right pulmonary artery are particularly susceptible to high-altitude pulmonary edema. The occurrence of high-altitude pulmonary edema was documented in a child with congenital absence of the right pulmonary artery. Improvement occurred only upon descent to low altitude. Physicians should be aware of this life-threatening condition in children ascending to high altitude, particularly in individuals with unilateral absence of a pulmonary artery.     

Common pulmonary vein atresia without anomalous pulmonary venous connection

Common pulmonary vein atresia without pulmonary venous connection is a rare form of congenital heart disease. No communication exists between the confluence of the pulmonary veins and the heart or a major systemic vessel. A case diagnosed antemortem is presented. Correct early diagnosis is imperative as surgery may be corrective.     

Liposteroid against refractory pulmonary haemorrhage in idiopathic pulmonary haemosiderosis

We describe two Japanese children with idiopathic pulmonary haemosiderosis (IPH), whose refractory haemorrhages were treated with an intravenous lipid emulsion containing dexamethasone (liposteroid). A 22-month-old boy and a 14-month-old girl have been observed with similar symptoms; periodic bouts of anaemia, reticulocytosis, diffuse infiltrates on chest X-ray and the finding of siderophages in sputum or gastric lavage fluid. The MRI of the lung was useful for the diagnosis. Methylprednisolone pulse therapy was successful in treating acute massive bleeding. Subsequent oral prednisolone could not prevent chronic recurrent haemorrhages. However, the intermittent administration of liposteroid (0.05 mg/kg/dose IV) led to a cessation of bleeding; the haemoglobin concentration rose to normal levels. This observation emphasizes the usefulness of liposteroid in the management of refractory IPH.     

Congenital pulmonary arteriovenous fistula producing pulmonary arterial steal syndrome

Summary This report describes a congenital pulmonary arterial steal syndrome manifested as cyanosis and acidosis in a newborn. A fistulous connection between the right pulmonary artery and a large, anomalous right common pulmonary vein stole blood from the pulmonary arteries. The anomaly was suspected because of a pericardiac shadow on frontal and lateral chest films, substantiated by M-mode echocardiogram, confirmed at cardiac catheterization with angiocardiography, and analyzed at postmortem examination. Supported in part by a grant from The Rose M. Badgeley Charitable Trust     

Intralobar pulmonary sequestration occurring without alteration of pulmonary parenchyma

Typical changes of lung sequestration, including the scimitar sign, were seen on plain films in the left lower lobe. At aortography vasculature of a pulmonary sequestration was seen located paravertebrally in the left posterobasal segment. The arterial supply arose from a division of the thoracic aorta above the diaphragm; venous drainage was to the pulmonary veins. No pulmonary parenchymal changes were detected in the sequestration after resection, nor was there an extrapleural component of the sequestration.     

Pediatric pulmonary CT-scanning

Forty three lung scans, obtained in 29 anaesthetized children, were evaluated and compared with 85 scans performed in 52 sedated children. Confluent high absorptive areas in the lower parts of the lungs were found in 35 (81%) of the scans performed in children under general anaesthesia but such areas were not found in the scans performed under sedation. — For general anaesthesia, halothane-N₂O-O₂ was used in all but one patient. The radiological changes are presumably due to a fall in functional residual capacity with consequent airway closure. — It is important not to misinterpret these anaesthesia-induced pulmonary changes which may obscure or mimic true pathological lesions, such as parenchymal and pleural metastases.     

Visualization of pulmonary vein obstruction by pulmonary artery wedge injection

Summary One of the major postoperative complications of total anomalous pulmonary venous connection is obstruction of the pulmonary veins. This event may be apparent immediately after surgery when it is usually due to congenitally obstructed veins or later when it may be the result of failure of commensurate growth of the left atrium-common vein anastomosis or of scarring at the anastomotic site. The exact location of the obstruction becomes, then, of paramount importance in deciding if the patient can be helped by further surgery. At cardiac catheterization, pulmonary artery wedge injection was the only angiographic technique that visualized the site and degree of pulmonary venous obstruction in the case reported here.