一氧化氮与缺氧性肺动脉高压

缺氧性肺动脉高压主要基于肺动脉和肺小动脉收缩以及肺血管结构改变,而缺氧损伤自主性血管扩张是肺血管收缩的原因之一。一氧化氮(nitric oxide,NO)是一种强有力的内源性血管舒张因子,它作为第二信使在肺内具有选择性扩张血管作用,是维持正常肺循环低压的重要而不可缺少的因素。此外,机体在低氧血症刺激下,内源性NO合成及释放障碍,参与了肺动脉高压的形成。本文对此作一综述。 1 NO的合成与代谢 NO是一种非常特殊的小分子,主要以气体形式存在,在水中的溶解度低,极易被氧化,半衰期2～30秒,但在无氧及酸性     

吸入一氧化氮治疗肺动脉高压的血药浓度监测

监测２９例肺动脉高压病人吸入一氧化氮（ＮＯ）治疗前后的血药浓度，并与吸入浓度的相关性进行比较。结果显示，成人组吸入ＮＯ３０ｍｉｎ、儿童组吸入ＮＯ２０ｍｉｎ的血浆浓度较基础值显著升高（Ｐ〈０．０５和Ｐ〈０．００１）；停吸后２小时，ＮＯ血浆浓度已恢复至治疗前水平（Ｐ〉０．０５）。吸入ＮＯ浓度与血药浓度相关性较差。提示ＮＯ疗效与血药浓度有关，但吸入浓度应控制在一定范围内，以避免毒副反应的发生。     

新生儿肺动脉高压的研究进展

肺动脉收缩压(polmonary arterial systolic pressure，PASP)超过30mmHg或肺动脉平均压(pulmonary arterial mean pressure，PAMP)超过20mmHg时，即表示有肺动脉高压存在(新生儿2周内，正常肺动脉压力可稍高，约为40mmHg左右)。常见的疾病有：先天性心脏病、新生儿持续性肺动脉压力(持续性胎儿循环)、缺氧性疾病(新生儿窒息、新生儿肺炎、支气管肺发育不良等)。近10余年来，在小儿肺动脉高压的发病机制及临床上无创诊断方法均取得了较好的效果。     

一氧化氮吸入治疗新生儿持续性肺动脉高压

一氧化氮吸入治疗新生儿持续性肺动脉高压刘敬陈自励（综述）作者单位：１０２５００北京市燕化医院儿科研究室（刘敬）；４３００７０武汉市湖北省妇幼保健院新生儿研究室（陈自励）１９８０年，Ｆｕｒｃｈｇｏｔ和Ｚａｗａｄｚｋｉ发现动脉血管的舒张作用有赖于内皮细胞...     

肺动脉高压治疗的研究进展

肺动脉高压治疗的研究进展浙江杭州市拱墅区红十字会医院李曙民浙江医科大学临床药理研究所卞如濂一般概念我国的慢性阻塞性肺病（ＣＯＰＤ）发病率极高，绝大多数的ＣＯＰＤ都发展为肺动脉高压（ＰＨ）和肺心病。ＰＨ是肺心病发生发展的病理生理基础，其脉压高低是影响肺...     

内皮素与肺动脉高压

自日本学者Yanagisawa等首次分离出内皮素(En-dothetin, ET)以来,有关ET的研究成为近年来的热点课题之一。目前已初步揭示了ET的结构、来源、分类、代谢、生物学特征,及影响ET合成、分泌的调节因素等。表明ET在许多疾病的发生中具有重要的生理和病理意义。本文就ET与肺动脉高压的关系进行综述。 1 内皮素及其生物学特性概述 ET是Yanagisawa等首次从培养的猪主动脉内皮细胞分离出来的一种血管活性多肽,由21个氨基酸组     

一氧化氮治疗肺心病肺动脉高压的多普勒超声评价

近年来许多学者对一氧化氮(NO)的研究掀起热潮,大多数作者认为NO可选择性扩张肺血管,从而降低肺动脉压,我们对12例肺心病患者用自身对照法进行了多普勒超声心动图评价.资料和方法一、病例12例肺心病患者均符合1980年全国第三次肺心病专业会议标准及超声心动图诊断标准,其中男性5例,女性7例,年龄47～76岁,平均62岁,咳喘病史5～40年,平均20年.二、药剂与仪器一氧化氮(NO)气体,浓度为800-1000PPM,化学发光法NO·Modle 8840型NO_2浓度监测仪,呼吸机及血气分析仪,美国惠普1500型彩色超声多普勒诊断仪.     

低浓度NO吸入对兔低氧性肺动脉高压的作用

目的 :探讨低浓度一氧化氮 (NO)吸入对兔低氧性肺动脉高压模型的作用。方法 :予家兔急性低氧性肺动脉高压模型先后吸入 2、 4、 6、 10、 2 0ppmNO ,通过左颈总动脉插管、右心室插管观察平均动脉压 (MAP)、右心室收缩压 (SRVP)及血气的变化。结果 :低氧通气使SRVP由 1 87± 0 2 9kPa升至 2 32± 0 2 7kPa。吸入 2ppmNO气体使SRVP显著降低。NO吸入过程中MAP保持不变。低氧通气使PaO2 显著下降 ,低氧通气同时吸入NO ,PaO2 无变化。结论 :吸入 2ppmNO气体即能选择性扩张肺血管。     

雾化吸入一氧化氮供体治疗新生猪急性低氧性肺动脉高压

目的探讨雾化吸入一氧化氮供体对新生猪急性低氧性肺动脉高压的作用和安全性。方法持续低氧(FiO2=0.1)1h建立急性低氧性肺动脉高压模型。18头新生猪造模后随机分成3组(每组6只):C组(生理盐水组)、NTG组(硝酸甘油组)和SNP组(硝普钠组),另6头新生猪设为S组(假手术组),作为对照。实验过程中连续监测平均股动脉压(MAP)和平均肺动脉压(MPAP),基础状态、缺氧1h、雾化结束时和雾化后0.5h测定动脉血气分析,雾化结束时测定全血高铁血红蛋白(MetHb)水平和血浆NO代谢产物(NO-2NO-3)的含量。结果缺氧1h后,C组、NTG组和SNP组的MPAP均较S组显著升高(P<0.01);雾化结束时,NTG组和SNP组的MPAP较C组显著下降(P<0.05)。在相同时点,4组新生猪的MAP差异无显著性(P>0.05)。雾化吸入结束时,4组新生猪的全血MetHb和血浆NO浓度差异无显著性(P>0.05)。雾化结束后,未发现有反跳性肺动脉高压。结论雾化吸入NTG或SNP能选择性地降低急性低氧引起的肺动脉高压。     

内皮型一氧化氮合酶基因转移对大鼠慢性低氧性肺动脉高压的预防作用

目的 探讨内皮型一氧化氮合酶(eNOS)基因转移对大鼠慢性低氧性肺动脉高压(CHPH)的预防作用.方法 雄性Wistar大鼠24只被随机分为常氧(N)组、低氧(H)组、低氧LacZ(H-LacZ)组和低氧eNOS(H-eNOS)组,每组6只.经气道转基因,H-eNOS组注入5×1012 pfu/L AdCMVceNOS 50μl,重复12次,H-LacZ组注入等量AdCMVLacZ,其他两组注入等量生理盐水;3 d后建立大鼠CHPH模型.低氧结束后(2周)检测血动力学指标[体循环平均动脉压(MSAP)、心率(HR)和平均肺动脉压(MPAP)],肺小血管肌化程度(肺小血管中肌型动脉所占比例)和右心室肥厚指数[右心室/(左心室+室间隔)],并行肺组织eNOS蛋白检测及环磷酸鸟苷(cGMP)和一氧化氮(NO)含量测定.结果 H-eNOS组大鼠MPAP、右心室肥厚指数和肺小血管肌化程度明显低于H组与H-LacZ组,明显高于N组(P均<0.01);各组大鼠HR和MSAP比较差异均无统计学意义(P均>0.05);H和H-LacZ组eNOS蛋白含量明显高于N组,低于H-eNOS组(P均<0.01);H组和H-LaeZ组大鼠肺组织NO含量明显低于N组,而H-eNOS组明显高于其他3组(P<0.05或P<0.01);N、H和H-LacZ组大鼠肺组织cGMP含量明显低于H-eNOS组(P均<0.01),且3组间比较差异无统计学意义(P均>0.05).结论 经气道eNOS基因转移,可增强肺组织eNOS活性,增加NO/cGMP含量,减少大鼠CHPH的发生率.     

Combination of inhaled nitric oxide and intravenous prostacyclin for successful treatment of severe pulmonary hypertension in a patient with acute respiratory distress syndrome

Objective: To investigate the combination of inhaled nitric oxide (iNO) and intravenously administered prostacyclin (i. v. PGI₂) in a patient with severe pulmonary hypertension and acute respiratory distress syndrome (ARDS). Design: Single case study. Setting: Intensive care unit of a university hospital. Methods: In an ARDS patient with severe pulmonary hypertension, gas exchange and hemodynamics were measured during combined treatment with iNO and i. v. PGI₂. On two subsequent days, a protocol consisting of four 20-min periods was performed: baseline, 10 ppm iNO, 10 ppm iNO plus 4 ng kg⁻¹ min⁻¹, and 4 ng kg⁻¹ min⁻¹ PGI₂ alone. At the end of each period hemodynamic and gas exchange data were obtained. Results: The combination of iNO and i. v. PGI₂ resulted in a marked decrease in pulmonary artery pressure and a concomitant increase in cardiac output which was more pronounced than the effect of either drug alone. During iNO, as well as during the combination of iNO and i. v. PGI₂, oxygenation was improved, whereas during i. v. PGI₂ alone oxygenation was worse than baseline. Conclusion: We conclude that the combination of iNO and i. v. PGI₂ might be more useful than either drug alone when severe pulmonary hypertension leading to impaired right ventricular function is present in ARDS. A systematic study of this observation is warranted. Received: 19 November 1998 Final revision received: 18 February 1999 Accepted: 12 April 1999     

超声心动图评价肺动脉高压患者右心室局部及整体收缩功能研究进展

肺动脉高压是指肺动脉压力升高超过一定界值并导致右心功能衰竭的综合征,早期识别、准确评价右心功能障碍在PH患者的诊断、治疗及预后中起重要作用。虽然导管测压是金标准,但是超声是无创评估PH的重要手段,组织多普勒、实时三维超声心动图以及斑点追踪成像等超声新技术可以定性和定量评价PH患者的右心室结构和功能。     

Endothelial nitric oxide synthase (NOS) is upregulated in rapid progressive pulmonary hypertension of the newborn

Objective To provide evidence for the upregulation of endothelial nitric oxide synthase (eNOS) or inducible nitric oxide synthase (iNOS) in the assumed imbalance in the pathophysiology of rapid progressive pulmonary hypertension of the newborn (RPPHN), which is characterized by abnormal hypertrophy of the pulmonary arterioles and arteries leading to increased pulmonary vascular resistance. Furthermore, to determine the cellular source and topographic distribution of eNOS and iNOS.Material and Methods Lung biopsies were taken from two term neonates with clinical and echocardiographic evidence of RPPH and of three controls. Biopsies were obtained at an early stage of the disease as well as at post mortem and examined immunohistochemically for the presence of eNOS, iNOS and nitrotyrosine.Results The endothelial cells of pulmonary arterioles stained significantly for eNOS protein in RPPHN patients. This was not the case in the control infants. There were no differences for nitrotyrosine or iNOS between RPPHN patients and controls.Conclusion Rapid progressive pulmonary hypertension of the newborn leads to compensatory induction of eNOS synthesis specifically in endothelial cells of the pulmonary arterioles. This mechanism of compensation can lead to delayed presentation of RPPHN during the late neonatal period. Exogenous inhaled nitric oxide therapy does not lead to suppression of the endogenous synthesis of nitric oxide.     

Relief of severe pulmonary hypertension after closure of a large ventricular septal defect using low dose inhaled nitric oxide

A 16-month-old girl developed severe pulmonary hyptertension after closure of a large ventricular septal defect. All conventional therapeutic measures failed; an attempt to add nitric oxide at a continous low dose to the inspired gas allowed resolution of pulmonary hypertension and low cardiac output. This report documents that continuous inhalation of low dose nitric oxide is capable of selective resolution of pulmonary hypertension following cardiac surgery for a large septal defect in a child. This suggests that a transient dysfunction in the release of nitric oxide by the pulmonary endothelial cell is responsible for the vasoconstriction.     

超声新技术评价肺动脉高压患者右心房功能研究进展

肺动脉高压(pulmonary hypertension,PH)是以肺部循环阻力在致病因素作用下持续上升,导致肺动脉收缩压(pulmonary artery systolic pressure,PASP)持续性上升,伴随着不可逆性的肺血管重构,继而损害右心系统功能甚至死亡为临床特征的一组病理生理综合征。右心功能是决定PH患者预后的关键因素[1],右心房作为右心系统不可或缺的一部分对维持右室充盈起重要作用,积极评估右心房的结构和功能变化对PH患者的监测和预后至关重要。现有的评价右心房功能的超声新技术主要分为两大类：容量性评价右房泵功能和非容量性评价右房机械功能。本文就超声新技术在评价PH患者右心房功能的应用进展方面作以下综述。     

肾血管性高血压对诱导型一氧化氮合酶表达及活性的影响

目的通过测定肾血管性高血压大鼠血管及肾组织诱导型一氧化氮合酶（iNOS）活性及表达的变化情况,探讨血压与iNOS间的关系。方法运用肾动脉不全结扎方法制备SD大鼠肾血管性高血压模型,并应用Greiss反应、L-精氨酸同位素标记法及Westernblot等分别测定一氧化氮的终产物——尿中NO