机械呼吸式一氧化氮吸入疗法

目的；低浓度一氧化氮吸入可选择性降低肺动脉高压，对于不能自主呼吸的病人，一氧化氮吸入法的机械呼吸方式的推广，是十分必要的。方法 采用ＮＥＷＰＯＲＴ１５０岗儿呼吸机，通过改变治疗气中ＮＯ浓度，观察小儿肺动脉高压的改善状况。结果：９例患儿吸入１５－２０ｐｐｍＮＯ，７例低氧症状改善，吸入３０分钟后，动脉血氧显著增加。     

正常人脑血管反应和储备能力的评价

目的探讨改进的CO2麻醉气囊吸入法评价正常人脑血管反应和储备能力,建立正常参考值.方法 70例体检健康人入选本试验组.常规TCD检查后,进入TCD8.0 CO2反应监测软件,取双侧MCA作监测血管,经改进的麻醉呼吸气囊接可充气呼吸面罩,使受检者吸入5% CO2和95% O2混合气体1min诱发高碳酸血症,经过度换气试验诱发低碳酸血症,计算试验前后血流速度变化百分比.结果 5% CO2吸入1 min后,Ⅰ、Ⅱ两年龄组正常人血流速度的增加率分别34.23±11.29% 和35.15±10.35%;过度换气后,Ⅰ、Ⅱ两组正常人血流速度的下降率分别为39.93±7.59%和43.37±10.23%;两组之间血流速度变化率无显著差异(p>0.05).结论正常人脑血管反应和储备能力随着年龄的增加而降低;CO2麻醉气囊吸入法和过度换气法评价脑血管反应和储备能力安全可靠.     

一氧化碳吸入装置的设计与实现

目的一氧化碳(carbon monoxide,CO)是一种重要的内源性介质,可用于治疗新生儿持续肺动脉高压、急性肺损伤等严重疾病。但目前有关一氧化碳吸入装置的报道较少,因此本文设计并实现了一种与呼吸机联用的一氧化碳吸入装置以满足临床需求。方法通过气体稀释公式计算出在治疗条件下CO标气的流量,并由转子流量计控制CO标气送入呼吸回路,采用CO电化学传感器对进入患者前的治疗气中CO浓度进行检测,具有实时监测、显示浓度、超标声光报警等功能,并与呼吸机联用后检验了该装置的示值误差和响应时间。结果该装置的示值误差为2.2%,响应时间平均为23.5 s,能满足临床实验的需求。结论本文所研发的与呼吸机联用吸入装置的浓度监测范围、输出流量、响应时间及显示精度等技术参数满足预期的设计要求。     

饮茶对狗急性低氧性肺动脉高压的影响—前列腺素的作用

本实验给狗胃内灌注红茶和绿茶,观察了饮茶对狗血流动力学和急性低氧性肺动脉高压的影响,同时探讨了前列腺素在其中的作用。实验结果表明红茶显著抑制吸入低氧气体引起的肺动脉高压和血浆血栓素A_2(TXA_2)的升高,但绿茶对急性低氧性肺动脉高压和缺氧时血浆TXA_2、前列环素(PGI_2)的变化无明显影响。本文结果提示饮红茶可能有利于低氧性肺动脉高压的防治,其作用与抑制缺氧时TXA_2的合成和/或释放有关。     

一氧化氮吸入疗法治疗新生儿持续肺动脉高压的副作用研究

目的：探讨一氧化氮（NO）吸入疗法治疗新生儿持续肺动脉高压的疗效及副作用。方法：对24例新生儿持续肺动脉高压患儿给予NO吸入疗法治疗,观察全身氧合情况的变化,同时持续监测心率、血压,吸入前后检测血高铁血红蛋白定量并监测凝血功能的改变。结果：24例患儿中19例（79.2%）治疗后氧合情况显著改善,监测收率、血压无明显改变,高铁血红蛋白定量增高均在可以接受的范围内,凝血功能无明显改变。结论：NO中入疗法治疗新生儿持续肺动脉高压有显著疗效,且未见明显副作用。     

正常人脑血管反应和储备能力的评价

目的　探讨改进的CO2 麻醉气囊吸入法评价正常人脑血管反应和储备能力 ,建立正常参考值 .方法　 70例体检健康人入选本试验组 .常规TCD检查后 ,进入TCD8.0CO2 反应监测软件 ,取双侧MCA作监测血管 ,经改进的麻醉呼吸气囊接可充气呼吸面罩 ,使受检者吸入 5 %CO2 和 95 %O2 混合气体 1min诱发高碳酸血症 ,经过度换气试验诱发低碳酸血症 ,计算试验前后血流速度变化百分比 .结果　 5 %CO2 吸入 1min后 ,Ⅰ、Ⅱ两年龄组正常人血流速度的增加率分别 34.2 3± 11.2 9%和 35 .15± 10 .35 % ;过度换气后 ,Ⅰ、Ⅱ两组正常人血流速度的下降率分别为 39.93±7.5 9%和 4 3.37± 10 .2 3% ;两组之间血流速度变化率无显著差异 (p >0 .0 5 ) .结论　正常人脑血管反应和储备能力随着年龄的增加而降低 ;CO2 麻醉气囊吸入法和过度换气法评价脑血管反应和储备能力安全可靠     

二维斑点追踪技术评估阻塞性睡眠呼吸暂停综合征患者的右心室收缩功能

目的探究二维斑点追踪技术评估阻塞性睡眠呼吸暂停综合征患者的右心室收缩功能。方法 40例阻塞性睡眠呼吸暂停综合征患者分为伴肺动脉高压(PH)组和未伴PH组(每组20例),另组为30例正常体检者。均给予二维斑点追踪技术进行右心室收缩功能评估。结果阻塞性睡眠呼吸暂停综合征患者在右室舒张末内径、右室收缩末内径、室间隔厚度、右室后壁厚度、射血分数上与健康体检者存在显著差异(P 0. 05),阻塞性睡眠呼吸暂停综合征伴PH组在右室舒张末内径、右室收缩末内径、室间隔厚度、右室后壁厚度上均比其它二组高(P 0. 05),在射血分数上显著比其它两组低(P 0. 05)。结论将二维斑点追踪技术应用于阻塞性睡眠呼吸暂停综合征患者时,能评估右心室结构和功能,值得应用与推广。     

雾化吸入硝酸甘油治疗新生猪急性低氧性肺动脉高压和心肌损害的研究

目的： 探讨雾化吸入硝酸甘油（NTG）对新生猪急性低氧性肺动脉高压和心肌损害的疗效和安全性。方法: 24头上海种新生白猪建立急性低氧性肺动脉高压和心肌损害的模型。将动物随机分成4组：sham组（假手术组）；model组（模型组）；N1组（缺氧结束后雾化吸入NTG 0.5 h）和N2组（缺氧状态 0.5 h 后即雾化吸入NTG 0.5 h）。实验过程中连续监测平均动脉压（MAP）和平均肺动脉压(MPAP)，间断监测血清肌酸激酶心肌同功酶（CK-MB）、肌钙蛋白I（cTnI）浓度，TUNEL法检测心肌细胞凋亡,免疫组化染色检测心肌组织肌红蛋白(Mb)及心肌细胞缝隙连接蛋白Cx43的含量。结果: 缺氧 1 h 后，N2组的MPAP显著低于model组（P<0.01）；缺氧结束后 0.5 h，N1组的MPAP显著低于model组（P<0.05）。4组新生猪在相同时点的MAP差异无统计学意义（P>0.05）。缺氧结束后 5 h，N1和N2组的CK-MB与model组差异无统计学意义（P>0.05）；N1和N2组的cTnI的含量均显著低于model组（P<0.01）。N1和N2组的心肌细胞凋亡指数显著少于model组（P<0.05）；心肌Mb在N1和N2组的表达显著强于model组（P<0.01）；心肌Cx43在N1和N2组的表达也显著强于model组（P<0.05）。结论: 缺氧同时或缺氧后雾化吸入NTG均能选择性地降低急性低氧引起的肺动脉高压，对心肌也有一定的保护作用。     

肺动脉高压动物模型的理论研究及其制备特点

背景:建立肺动脉高压动物模型,对其深入研究有助于推动临床对肺动脉高压诊治水平的不断提高。目的:总结与探讨各种肺动脉动物模型的制备、病理生理学特点以及对临床肺动脉高压的模拟性。方法:应用计算机检索PubMed数据库1975-01/2009-09期间相关文章,检索词为"pulmonary hypertension、animal model",同时检索中国期刊全文数据1990-01/2009-09期间的相关文章,检索词为"肺动脉高压,动物模型"。纳入外科手术制作肺动脉高压动物模型的研究、药物注射制作肺动脉高压动物模型的研究、有新生内膜形成的肺动脉高压动物模型研究、肺动脉高压动物模型与临床肺动脉高压患者的病理生理对比的研究、肺动脉高压动物模型的药物干预研究。结果与结论:已知的肺动脉高压动物模型建立方法包括.外科手术建立分流术、野百合碱注射、低氧吸入法等经典方法,以及近年报道的几种有新生内膜产生的重度肺动脉高压模型。此类模型建立经过了不断地改进,为了解肺动脉高压的细胞及分子病理学机制提供了帮助,但尚不明确这些模型能在多大程度模拟临床肺动脉高压的细胞和分子发生机制,因此仍不清楚哪类模型更能代表临床肺动脉高压的病理机制。     

氨茶碱对缺氧动物吸入NO肺动脉高压反弹的预防效果观察

目的:评价氨茶碱对缺氧性动物吸入NO肺动脉高压反弹的预防作用。方法:采用右心漂浮导管检测法,由八导生理记录仪记录肺动脉平均压(mPAP),并监测呼吸、心率及动脉血氧分压变化。结果:急性缺氧猪吸入10^-5NO后,mPAP明显下降,突然停止吸入NO而改吸室内空气后,下降的mPAP逐渐回升,5min时恢复到吸入NO前水平,10min时已明显高于吸入NO前水平,与此同时,缺氧动物血氧分压反较吸入NO前低;而当急性缺氧猪在停止吸入NO的同时,静脉推注氨茶碱后,虽然下降的mPAP有所回升,但回升速度明显低于对照组,在停止吸入NO30min时仍低于吸入NO前水平。结论:氨茶碱对缺氧性动物吸入NO肺动脉高压反弹有明显的预防作用。     

Sleep apnea and pulmonary hypertension

Summary The pulmonary artery pressure values of 65 patients with sleep apnea syndrome were measured at rest and during ergometer exercise up to 100 W. Pulmonary hypertension at rest was found in 13, and during exercise in 31 more patients. Only 8 patients with pathological pressure findings suffered from pulmonary hypertension in combination with a pulmonary or cardiac disease. In the other 36 patients, no indication of a primary cause of pulmonary hypertension apart from sleep apnea syndrome could be found. Out of the 65 patients, 11 with a finding of more than 20 apnea episodes per hour's sleep underwent polysomnographic recordings in the sleep laboratory. The hemodynamic parameters were continuously measured. All 11 patients had a finding of severe sleep apnea with more than 300 apnea episodes during the night of recording. In 6 patients, the appearance of apnea episodes was accompanied by only moderate changes in pulmonary artery pressure. In 5 patients, there were critical increases in pulmonary artery pressure, which went along with increases in cardiac output and in pulmonary capillary wedge pressure. Increases in pulmonary vascular resistance were established in 3 out of these 5 patients, and a slight decrease in 2. The mechanism of hypoxic vasoconstriction of the pulmonary arteries may account for the pressure increases in 3 of our patients, but fails to explain the findings in the other 2 patients. Nocturnal changes in pulmonary artery pressure in patients with sleep apnea may therefore have different causes. Pulmonary hypertension constitutes a severe complication in patients with sleep apnea. As 55% of all sleep apnea patients were found to suffer from pulmonary hypertension without any indication of a primary pulmonary or cardiac disease, the possibility that pulmonary hypertension results should not be underestimated in patients with suspected sleep apnea syndrome. Measurements of the pulmonary artery pressure must therefore be included in the examination regimen of such patients.Abbreviations ECG electrocardiogram - REM rapid eye movement     

贝前列素钠治疗肺源性心脏病肺动脉高压的临床研究

目的:观察贝前列素钠治疗肺源性心脏病(肺心病)肺动脉高压的临床疗效。方法:将68例肺心病急性发作期患者随机分为对照组(n=31)和贝前列素钠组(n=37)。两组患者均给予抗感染、止咳、化痰、平喘、强心利尿等常规治疗,贝前列素钠组在上述治疗的基础上加口服贝前列素钠治疗。比较两组疗效和外周动脉压(PABP)、肺动脉压(PAP)、左室射血分数(LVEF)、血脑钠肽(BNP)、血气[酸碱度(pH),氧分压(PaO2)、二氧化碳分压(PaCO2)、血氧饱和度(SaO2)]及血清C反应蛋白(CRP)、内皮素-1(ET-1)、一氧化氮(NO)水平变化。结果:贝前列素钠组总有效率明显高于对照组(94.59%vs 77.42%,P0.05),显效率也显著高于对照组(48.65%vs 16.12%,P0.01)。治疗后两组PAP、CRP、ET-1、NO、BNP、血气指标较治疗前均明显改善(P0.05或P0.01);贝前列素钠组较对照组PAP、PaCO2、ET-1、BNP降低更明显(P0.01),PaO2、SaO2、NO升高更显著(P0.01)。结论:贝前列素钠可以明显降低肺心病肺动脉高压患者肺动脉压,改善心功能,这可能与其降低ET-1和提高NO水平有关。     

Präkapilläre pulmonale Hypertonie

Precapillary pulmonary hypertension (PH) is defined by hemodynamic variables (i.e., a mean pulmonary artery pressure ≥?25 mmHg in the presence of normal pulmonary capillary wedge pressure). The relationship between PH and sleep-disordered breathing is more complex than initially thought. Earlier studies have shown that obstructive sleep apnea (OSA) can induce chronic daytime PH. It has only recently been recognized that OSA is frequently associated with acute PH in the setting of pulmonary embolism and that chronic PH can lead to the development of central sleep apnea/Cheyne–Stokes respiration.     

Cardiovascular risk among adults with obstructive sleep apnea syndrome

Cardiovascular diseases and sleep-disordered breathing have been recognized as a public health problem in Mexico and worldwide. These two groups of disorders are closely associated and the evidence accumulated over the last 25 years indicates that obstructive sleep apnea syndrome (OSAS) is an independent risk factor in systemic arterial hypertension, coronary artery disease and stroke. Other associations have also been described, linking these disorders with pulmonary hypertension, cardiac arrhythmias, sudden death during sleep and congestive heart failure. Treatment with continuous positive airway pressure in patients with OSAS has proven to be an efficient primary and secondary cardiovascular prevention strategy. This article reviews the epidemiological evidence that links OSAS with increased cardiovascular risk, and proposes strategies designed to address this growing health problem.     

Apnea testing with continuous positive airway pressure for the diagnosis of brain death in a patient with poor baseline oxygenation status

Apnea testing is a key component in the clinical diagnosis of brain death. Patients with poor baseline oxygenation may not tolerate the standard 8-10 min apnea testing with oxygen insufflation through tracheal tube. No studies have assessed the safety and feasibility of other methods of oxygenation during apnea testing in these types of patients. Here, we safely performed apnea testing in a patient with baseline PaO₂ of 99.1 mm Hg at 100% oxygen. We used continuous positive airway pressure (CPAP) of 10 cm of H₂O and 100% oxygen at the flow rate of 12 L/min using the circle system of anesthesia machine. After 10 min of apnea testing, PaO₂ decreased to 75.7 mm Hg. There was a significant rise in PaCO₂ and fall in pH, but without hemodynamic instability, arrhythmias, or desaturation. Thus, the apnea test was declared positive. CPAP can be a valuable, feasible and safe means of oxygenation during apnea testing in patients with poor baseline oxygenation, thus avoiding the need for ancillary tests.     

Arterial stiffness increases during obstructive sleep apneas

STUDY OBJECTIVES: Obstructive sleep apnea (OSA) appears to be an independent risk factor for diurnal systemic hypertension, but the specific biologic markers for this association have not been well established. Increased arterial stiffness is an important measure of increased left ventricular load and a predictor of cardiovascular morbidity and may precede the onset of systemic hypertension in humans. However, arterial stiffness has not been measured in association with obstructive apneas in patients with OSA, nor related to systemic blood pressure (BP) activity in this setting. Our objective was to test the hypothesis that arterial stiffness may be utilized as a sensitive measure of arterial vasomotor perturbation during obstructive events in patients with OSA, by demonstrating that (1) arterial stiffness increases acutely in association with obstructive apnea and hypopnea, and that (2) such increased stiffness may occur in the absence of acute BP increase. DESIGN: Prospective, cross-sectional. SETTING: A tertiary-care university-based sleep and ventilatory disorders center. PATIENTS: Forty-four normo- and hypertensive adult patients (11 women, 33 men) with polysomnographically diagnosed moderate to severe OSA. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Beat-to-beat BP was recorded from the radial artery by applanation tonometry during nocturnal polysomnography. Arterial augmentation index (AAI), a measure of arterial stiffness, was calculated as the ratio of augmented systolic BP (SBP) to pulse pressure and expressed as a percentage for the following conditions: awake, the first 10 ("early apnea") and last 10 ("late apnea") cardiac cycles of obstructive events, and the first 15 cardiac cycles following apnea termination ("post apnea"). Mean AAI (+/-SD) for the group was significantly increased during NREM sleep from early apnea to late apnea (12.02 +/- 2.70% vs 13.35 +/- 3.54%, p<0.05, ANOVA). During REM (analyzed in 20 patients), MI again significantly increased from early apnea to late apnea (11.75 +/- 2.81% vs 13.43 +/- 4.97%). Conversely, neither mean SBP nor mean arterial BP was significantly changed from early apnea to late apnea in NREM (SBP 130 +/- 14 mmHg vs 129 +/- 14 mmHg) or REM (SBP 128 +/- 22 mmHg vs 127 +/- 21 mmHg). CONCLUSIONS: Arterial stiffness increases acutely during obstructive apneas in both NREM and REM sleep, in the absence of measurable BP change. These data suggest that arterial stiffness may be a sensitive measure of acute arterial vasomotor perturbation in this setting and may have implications concerning cardiovascular sequelae in patients with OSA.     

结缔组织病相关的肺动脉高压研究进展

肺动脉高压是结缔组织病（CTD）的严重并发症之一。结缔组织病中最常受累的是系统性硬化症（SSc）,而混合性结缔组织病（MCTD）、系统性红斑狼疮（SLE）及炎性肌病包括多肌炎和皮肌炎也常被累及。结缔组织病相关的肺动脉高压引起的原因不仅是肺动脉的病变,慢性血栓的形成,自身免疫反应和肺间质病变也是引起肺动脉高压的原因之一。由于其症状出现晚且不典型,预后甚差,死亡率高,因此对结缔组织病相关的肺动脉高压早期诊断,及时合理的治疗十分重要。     

Involvement of phospholipase A2 pathway for the Indian red scorpion venom-induced augmentation of cardiopulmonary reflexes elicited by phenyldiguanide

The present study was conducted to examine the role of phospholipase A(2) and prostaglandins in Indian red scorpion (Mesobuthus tamulus; MBT) venom-induced augmentation of cardiopulmonary reflexes elicited by phenyldiguanide (PDG). Trachea, femoral artery and jugular vein were cannulated in urethane anesthetized adult albino rats. The effect of jugular venous injection of PDG on ECG, BP and respiratory activity were recorded. Injection of PDG (10 microg/kg) evoked tachypnea/apnea, bradycardia and hypotension lasting for 60s. After injecting MBT venom (100 microg/kg) for 30 min, the PDG evoked reflex responses were augmented by two times and increased the pulmonary water content in envenomed animals, significantly. The venom-induced augmentation of PDG reflex and the increase in pulmonary water content were blocked in animals pretreated with B(2) kinin receptor antagonist (Hoe 140; 2.32 microg/kg). These responses induced by venom were also blocked by a phospholipase A(2) antagonist (PACOCF(3); 1 mg/kg) and a prostaglandin synthase inhibitor (indomethacin; 10 mg/kg). The observations indicate that the venom-induced responses (augmentation of PDG reflex response and increased pulmonary water content) involve PLA(2)-prostaglandin pathway that is triggered by B(2) kinin receptors to sensitize the receptors located on the vagal C-fibres.     

Influence of age on L-type Ca2+ channels in the pulmonary artery and vein of spontaneously hypertensive rats

The influence of age on the density and localization of L-type Ca²⁺ channels was studied during development of hypertension in the pulmonary artery and vein of spontaneously hypertensive rats (SHR) and age-matched normotensive Wistar–Kyoto (WKY) rats by radioligand binding assay and light microscope autoradiography. SHR were examined at 6 weeks (juvenile, pre-hypertensive stage), 12 weeks (young, developing hypertension) and 24 weeks (mature, established hypertension). The dihydropyridine-type Ca²⁺ antagonist [³H]nicardipine was used as a radioligand. It was bound specifically to sections of rat pulmonary artery and vein. Dissociation constant (K_d) values were similar in WKY rats and SHR, whereas maximum density of binding sites (B_max) values increased in SHR in comparison with WKY rats. This increase was noticeable from the pre-hypertensive phase. The pharmacological profile of [³H]nicardipine binding was similar in different age groups of either normotensive and hypertensive rats. Quantitative analysis of autoradiographs from SHR revealed a progressive increase of silver grains in smooth muscle of tunica media and to a lesser extent in the adventitia of pulmonary artery but not of pulmonary vein from pre-hypertensive stage to developing hypertension. No further changes were observed in established hypertension. The above data indicate that the density of L-type Ca²⁺ channels of pulmonary arteries is increased in SHR. This augmentation after the pre-hypertensive phase suggests the occurrence of dysregulation of Ca²⁺ handling in the pulmonary vasculature of developing SHR.     

Mental stress increases right heart afterload in severe pulmonary hypertension.

Little is known about mental stress effects on the pulmonary circulation in health and disease. The current study was conducted to investigate whether pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR) would further increase during standardized mental stress testing in patients with severe pulmonary hypertension. The study was a prospective analysis of seven patients (average age: 40 years, range from 21 to 56 years) with severe pulmonary hypertension (primary: n = 4, secondary forms: n = 3; resting mean pulmonary artery pressure ranged between 48 and 65 mmHg). Right heart catheterization for the determination of PAP, pulmonary capillary wedge pressure (PCW) and cardiac output (CO) was clinically indicated (diagnostic workup, acute drug testing). Patients accomplished a standardized 10 min mental stress test (computer based, adaptive complex reaction-time task). Pulmonary haemodynamics during stress were compared to resting baseline. During mental stress mean PAP (+/- SEM) increased by 9.4 +/- 2.1 mmHg (P < 0.005). Pulmonary vascular resistance increased by 149 +/- 25 dyne s cm-5 (P < 0.001). Stroke volume decreased by 6.6 +/- 2.2 ml (P < 0.03). The data show that moderate mental stress increases right heart afterload in patients with severe pulmonary hypertension owing to elevation of PVR.