吸入一氧化氮降低烟雾吸入性损伤肺动脉高压的实验研究

烟雾吸入致肺组织细胞损伤后５ｍｉｎ，行肺灌洗机械通气４ｈ，观察２４。酹明，犬随机分为三组。烟雾吸入后，对照组单纯涓氧；治疗组吸氧加０．００４５％ＮＯ，连续监测１２ｈ血循环动力学化；正常组不致伤。     

一氧化氮与肺动脉高压

一氧化氮与肺动脉高压祁国奇综述郭斌审校肺动脉高压是许多疾病的严重并发症，虽然有许多药物能扩张肺血管，但缺乏选择性，易导致体动脉压下降，故限制了其在临床上的应用。有效治疗肺动脉高压一直困扰着临床，随着对血管内皮细胞研究的深入，发现内皮细胞在调节血管舒缩...     

一氧化氮对吸入性损伤中性粒细胞在肺内扣押的影响

吸入性损伤治疗的研究一直受到国内外的广泛关注 ,一氧化氮 (NO)降低肺动脉压已有较深入的研究[1] ,但对中性粒细胞 (PMN)在肺内扣押的影响报道较少。我们旨在观察烟雾吸入性损伤后吸入 2 0ppm的NO对大鼠PMN在肺内扣押的影响。一、材料与方法1.主要试剂及设备 :NO (80 2 ppm ,北京市华元气体化工有限公司 ) ;高纯度氮气 (N2 ,北京普莱克斯实用气体有限公司 ) ;髓过氧化物酶 (MPO )测试盒 (南京建成生物工程研究所 ) ;动物人工呼吸机DH 14 0B(浙江医科大学医学仪器实验厂 ) ;42C型氮氧化物分析仪。2 .实验动物 :雄性Wistar大鼠 88只…     

一氧化氮吸入法治疗肺动脉高压的研究进展

一氧化氮吸入法治疗肺动脉高压的研究进展朱兵谷天祥综述张显清审校继Ｉｇｎａｒｏ和Ｐａｌｍｅｒ等［１，２］发现并确认一氧化氮（ｎｉｔｒｉｃｏｘｉｄｅ，ＮＯ）就是血管内皮松弛因子（ｅｎ－ｄｏｔｈｅｌｉｕｍ－ｄｅｒｉｖｅｄｒｅｌａｘｉｎｇｆａｃｔｏｒ，ＥＤＲ...     

外源性一氧化氮治疗吸入性损伤的研究进展

吸入性损伤的主要致伤因素是烟雾而非热力 ,严重吸入性损伤时大量毒性物质进入体内 ,不但直接损伤呼吸道和肺实质 ,而且对心血管和中枢神经系统产生不良影响[1] 。临床已采用吸氧、气管切开、呼吸末正压通气 (ＰＥＥＰ)、高频通气措施等治疗吸入性损伤 ,但疗效欠佳[1] 。近年来     

肺动脉高压治疗进展

本文综述了肺动脉高压的病理生理和治疗方法，重点阐述了一氧化氮（ＮＯ）在各型肺动脉高压中的治疗作用。着重介绍了ＮＯ对心源性肺动脉高压、新生儿持续性肺动脉高压、ＡＲＤＳ的治疗作用以及使用ＮＯ中存在的问题。     

一氧化氮和腺苷联合治疗幼猪急性缺氧性肺动脉高压

目的　观察联合使用一氧化氮 (NO)和腺苷 (AD)对肺动脉高压的影响。方法　选用上海种白猪 10头 ,建立急性缺氧性肺动脉高压模型 ,采用分别使用吸入NO 2 0× 10 -6和静脉持续每分钟滴注AD 5 0 μg/kg体重 ,以及联合使用NO和AD的方式 ,在各时段进行各项血流动力学指标测定。结果　联合使用NO和AD ,平均肺动脉压力从 (37± 7)mmHg(1mmHg =0 .133kPa)降至 (2 0± 1)mmHg(P <0 .0 1) ,心排指数从 (2 .30± 0 .5 0 )L·min-1·m-2 升至 (2 .76± 0 .46 )L·min-1·m-2 (P <0 .0 5 )。结论　NO和AD联合治疗幼猪急性缺氧性肺动脉高压 ,在降低肺动脉压力的同时 ,还可增加心输出量。     

一氧化氮对肺动脉高压的作用观察

１７例先天性心脏病合并中到重度肺动脉高压小儿，吸入１６～６０ｐｐｍＮＯ２０ｍｉｎ，观察短时间吸入低浓度ＮＯ对肺动脉高压的作用，结果表明，吸入ＮＯ１ｍｉｎＰＡＰ开始下降，吸入１０ｍｉｎ后ＰＡＰ明显下降（Ｐ〈０．０５）停止吸入ＮＯ后５ｍｉｎＰＡＰ明显升高。实验中ＮＯ２浓度平均小于２ｐｐｍ，ＭｅｔＨｂ无明显增加，ＳＢＰ，ＤＢＰ，ＨＲ，ＳｐＯ２均无明显改变，提示ＮＯ是一种选择性的肺血管扩张药，临床低浓度短     

吸入一氧化氮治疗二尖瓣狭窄术后肺动脉高压的研究

目的 观察吸入ＮＯ治疗二尖瓣狭窄（ＭＳ）术后肺动脉高压（ＰＨ）的疗效。方法 ３０例ＭＳ二尖瓣置换（ＭＶＲ）术后ＰＨ病人,吸入２０ｐｐｍＮＯ３０ｍｉｎ后,停吸ＮＯ,１５ｍｉｎ后再吸入６ｐｐｍＮＯ,直至脱离呼吸机。采用Ｓｗａｎ－Ｇａｎｚ导管技术监测吸入前后的血液动力学及氧合指标。结果 吸入２０ｐｐｍＮＯ５ｍｉｎ后,肺动脉压、肺循环阻力、肺泡动脉血氧分压差及肺内分流率明显降低、中心静脉压、心率、心排血量     

肺动脉高压治疗进展

本文综述了肺动脉高压的病理生理和治疗方法,重点阐述了一氧化氮(NO)在各型肺动脉高压中的治疗作用。着重介绍了NO对心源性肺动脉高压、新生儿持续性肺动脉高压、ARDS的治疗作用以及使用NO中存在的问题。     

Uptake of inhaled nitric oxide in acute lung injury

Background: Despite the widespread use of inhaled nitric oxide (NO), little is known of its pulmonary uptake in patients with acute respiratory failure.
Methods: Fourteen patients with acute lung injury (ALI) and ongoing NO therapy were studied. Three doses of NO (5, 10 and 40 ppm) were given for 20 min and at each dose level the following parameters were recorded: minute ventilation, inspiratory NO cone, mixed expired NO cone, end-tidal NO cone, mixed expired CO₂ cone, end-tidal CO₂ cone and arterial CO₂ tension. Total uptake was calculated and correlated to the total amount of NO inhaled, the amount of NO administered to the alveolar space, and the amount of NO administered to the perfused alveolar space.
Results: About 35% of the total amount of NO delivered is taken up by the lungs, 70% of NO administered to the alveolar space is taken up, and 95–100% of the NO administered to perfused alveolar space is taken up. The size of the alveolar dead space varied between 10 and60% of the alveolar space. At 40 ppm of inhaled NO there was no difference between inspired and mixed expired NO₂ concentration, indicating that there is no significant NO₂ formation taking place in the lungs during NO inhalation at the concentrations studied.
Conclusions: Practically all NO administered to the perfused alveolar space is taken up. The total uptake differs from that of healthy persons probably because of differences in the alveolar dead space.     

Effects of inhaled nitric oxide on platelet-activating factor-induced pulmonary hypertension in dogs

Background: Platelet-activating factor (PAF), a lipid mediator released during endotoxin shock, induces pulmonary hypertension, systemic hypotension and cardiac dysfunction. In this study, we compared the effect of inhaled nitric oxide (NO) on PAF-induced pulmonary hypertension and NO metabolism with that on pulmonary hypertension induced by a stable thromboxane A₂ mimetic, U46619. Since PAF-induced hypotension might be mediated by NO, the effect of inhaled NO combined with an intravenously administered NO synthase inhibitor, N^G-nitro-L-arginine (L-NNA), on PAF-induced hemodynamic change was also investigated. Methods: In a total of 28 beagles anesthetized with pentobarbital the following substances were intravenously administered: PAF 0.56±0.30 μg·kg^-1·min^-1 (group PAF), L-NNA 10 mg·kg^-1+ PAF 0.04±0.03 μg·kg^-1· min^-1 (group L-NNA+ PAF), U46619 0.60±0.11 μg·kg^-1·min^-1 (group U46619) or L-NNA 10 mg·kg^-1+ U46619 0.61±0.23 μg·kg^-1· min^-1 (group L-NNA+U46619) to obtain a mean pulmonary arterial pressure (MPAP) of 25 mmHg. Nitric oxide was then inhaled at 5, 10, 20 and 40 ppm for 15 min at 15-min intervals in the order of increasing concentration. An additional 7 dogs (control group) inhaled NO at normal MPAP (17 mmHg). Hemodynamic and respiratory parameters, NOHb, NO₂^-+NO₃^-, and MetHb levels in blood were measured before and during NO administration. Results: In the control group, hemodynamic and respiratory values did not change significantly during NO administration. In group PAF, NO significantly reversed the PAF-induced pulmonary hypertension. PAF induced a marked systemic hypotension and cardiac output reduction, but these changes were not affected by inhalation of NO. L-NNA pretreatment markedly decreased the dose of PAF required to maintain a MPAP of 25 mmHg, and abolished the PAF-induced hypotension. In group L-NNA+PAF, the diminishing effect of inhaled NO on pulmonary vascular resistance (PVR) was significantly greater than that in group PAF. U46619 induced pulmonary hypertension and increases in blood pressure, intrapulmonary shunt and peak airway pressure. L-NNA pretreatment did not change the dose of U46619 required to maintain a MPAP of 25 mmHg. The effects of inhaled NO on PVR decrease were similar in groups U46619 and L-NNA+U46619. No NOHb was detected in any group. NO₂^-+NO₃^- concentration increased during NO administrations. There were no significant differences in NO₂^-+NO₃^-concentration among groups. Conclusions: Inhaled NO at the dose of 5–40 ppm effectively reversed PAF-induced pulmonary hypertension, especially following pretreatment with L-NNA. Inhaled NO did not affect PAF-induced hypotension or cardiac dysfunction. These findings indicate that low concentrations of inhaled NO may be useful in reversing pulmonary hypertension in the endotoxemia where PAF may be one mediator.     

Effect of inhaled nitric oxide on pulmonary vascular hyperpermeability in sheep following smoke inhalation

Smoke inhalation increases mortality and morbidity in burn patients. We have reported that smoke inhalation increases lung lymph flow, an index of pulmonary transvascular fluid flux and decreases reflection coefficient, an index of microvascular permeability to protein. Nitric oxide has been reported to decrease microvascular permeability to protein. We hypothesize that inhaled nitric oxide decreases pulmonary microvascular hyperpermeability following smoke inhalation. Sheep were prepared for study with a chronic lung lymph fistula, Swan-Ganz, left atrial, and femoral arterial catheters. Occluders were placed on pulmonary veins to measure reflection coefficient. All animals were insufflated with 4 × 12 breaths of cotton smoke. Sheep were randomly divided into two groups: NO (injured, treated with nitric oxide (40 ppm) inhalation, n = 6) and control (injured, not treated, n = 6). Nitric oxide inhalation was started 22 h after the insult. Control animals showed an increase in lung lymph flow, and lung water content. These changes were associated with marked increase in pulmonary microvascular resistance, pulmonary artery pressure, and decrease in reflection coefficient. Nitric oxide inhalation ameliorated the above-mentioned pathological changes. The results suggest that nitric oxide inhalation has potential for beneficial effect in the treatment of patients suffering from smoke inhalation.     

吸入一氧化碳对急性缺氧性肺动脉高压及缺氧性肺损伤的影响

目的 研究吸入一氧化碳(CO)对急性缺氧性肺动脉高压及缺氧性肺损伤的影响。方法 30只大鼠随机分为三组：对照组(n＝10)：吸入21％O2 30min；缺氧组(n＝10)：吸入10％O2与90％N2的缺氧混合气30min;CO组(n＝10)：吸入100ppm CO与10％O2 90％N2的混合气30min。随后取动脉血进行血气分析及碳氧血红蛋白测定，并测定血浆丙二醛(MDA)浓度及红细胞超氧化物歧化酶(SOD)的活性，放血处死大鼠后，速取右肺肺组织样本，戊二醛磷酸缓冲液固定后，采用透射电镜检查肺超微结构的变化。结果 与对照组比较，缺氧组平均肺动脉压(MPAP)明显升高，MDA水平增加，SOD活性降低，肺超微结构发生了病理改变；与缺氧组比较，CO组MPAP明显下降，PaO2明显增加，MDA水平下降，SOD活性升高，肺超微结构明显改善。结论 吸入CO可改善缺氧大鼠的氧合，降低肺动脉压，减少氧自由基产生，从而减轻了急性肺损伤。     

Successful treatment of chronic thromboembolic pulmonary hypertension with inhaled nitric oxide after right ventricular thrombectomy

We report a case of a 42-year-old male with chronic thromboembolic pulmonary hypertension. His preoperative examination revealed severe hypoxemia (PaO₂ 48 mmHg, PaCO₂ 34 mmHg in room air), a mass in the right ventricle and severe pulmonary hypertension (pulmonary arterial pressure 70/33 mmHg). We successfully performed right ventricular thrombectomy to prevent further embolization from the right ventricular thrombus. Using inhaled low dose nitric oxide (NO) during perioperative period, weaning from cardiopulmonary bypass and ventilator were easily done. In this case, inhaled NO was successfully administered for the perioperative management of chronic pulmonary hypertension.     

多巴酚丁胺对吸入NO降低缺氧性肺动脉高压作用量效关系的研究

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先天性心脏病术后肺动脉高压的一氧化氮吸入治疗

目的　探讨先天性心脏病(先心病)术后肺动脉高压(肺高压)病儿吸入一氧化氮(NO)的适应证、避免毒副作用等。方法　选择31例先心病术后传统治疗无效的、难治的反应性肺高压或肺高压危象病儿,给予NO吸入治疗。试验分NO吸入前、中、后3个阶段,各阶段均进行各项血液动力学指标的测定。结果　吸入不同浓度NO［10～80百万分之体积(ppm)］后,平均肺动脉压力和体肺循环压力之比分别降低了34.8%和45.0%(P＜0.01),有效率为87.1%;吸入NO后二氧化氮、高铁血红蛋白含量明显高于吸入前(P＜0.05),但仍在允许范围。结论　吸入NO可明显降低先心病术后难治的反应性肺高压或肺高压危象病儿的肺动脉压力和肺血管阻力,临床上未发现明显的毒副作用。因此,NO是一种有效、安全、理想的肺血管扩张剂。