吸入一氧化氮对烟雾吸入性损伤犬肺组织含水量的影响

目的：观察吸入一氧化氮（ＮＯ）对烟雾吸入性损伤犬肺组织含水量的影响。方法：２１只犬随机分为３组：烟雾吸入后单纯吸氧〔氧浓度（ＦｉＯ２）０．４５〕为对照组（８只）；吸氧（ＦｉＯ２０．４５）＋０．００４５％ＮＯ为治疗组（９只），按时相点采血标本；正常组（４只）不致伤，用于建立组织学对照。动脉血浆胶体渗透压（ＣＯＰ）行多个样本均数间方差分析；支气管肺泡灌洗液（ＢＡＬＦ）中ＣＯＰ和蛋白质含量行两样本均数ｔ检验。结果：吸入ＮＯ治疗组血浆ＣＯＰ比对照组升高（Ｐ＜０．０５）；ＢＡＬＦ中ＣＯＰ比对照组略降低（Ｐ＞０．０５），而ＢＡＬＦ中蛋白质含量比对照组明显降低（Ｐ＜０．０５）；肺组织含水量略低于对照组（Ｐ＞０．０５）。结论：吸入ＮＯ对烟雾吸入性损伤犬肺组织含水量有减轻趋势，但尚无显著的效果，对其病理转归的影响仍难以定论，有待进一步深入研究。     

犬烟雾吸入性损伤吸入一氧化氮肺脏病理改变与肺能量代谢的变化

目的：评价犬烟雾吸入性损伤吸入一氧化氮（ＮＯ）肺脏病理改变与肺组织能量代谢的变化。方法：２１只犬随机分为３组，烟雾吸入损伤后，对照组（ｎ＝８）单纯吸氧（ＦｉＯ２，０．４５），治疗组（ｎ＝９）吸氧（ＦｉＯ２，０．０４５）＋０．００４５％（４５ｐｐｍ）ＮＯ，正常组（ｎ＝４）不致伤，用于建立病理和组织学对照。实验终点进行肺组织学和病理形态学检测。结果：对照组ＡＴＰ含量和能量负荷（ＥＣ）显著低于正常和治疗组（Ｐ＜０．０１），ＡＤＰ和ＡＭＰ含量明显低于正常组（Ｐ＜０．０５），而与治疗组相比无显著差别（Ｐ＞０．０５）；肺脏光镜和电镜病理所见，治疗组病理性改变程度较对照组轻。结论：在烟雾吸入性损伤犬模型中，吸入ＮＯ可不同程度改善肺组织能量代谢，肺脏病理形态改变也有一定程度减轻，表明治疗方法有一定效果     

吸入一氧化氮改善烟雾吸入性损伤犬肺通气功能的意义

目的评价吸入一氧化氮（ＮＯ）对犬烟雾吸入性损伤肺通气功能改善的效果。方法烟雾吸入伤后，将１７只犬随机分为２组，对照组（ｎ＝８）单纯吸氧（ＦｉＯ２，０．４５），治疗组（ｎ＝９）吸氧（ＦｉＯ２，０．４５）＋０．００４５％（４５ｐｐｍ）ＮＯ，连续监测１２小时血气变化；并按时相点抽血检测有关指标。数据行多个样本均数间方差分析。结果吸入ＮＯ治疗组ＰａＣＯ２、呼吸指数（ＲＩ）、肺泡死腔率（ＶＤ／ＶＴ）、肺动脉分流率（ＱＳ／ＱＴ）和碳氧血红蛋白（ＨｂＣＯ）含量比对照组均有不同程度的下降（Ｐ＜０．０５～０．０１），而动脉血浆亚硝酸盐（ＮＯ－２）水平则明显高于对照组（Ｐ＜０．０１）。结论吸入ＮＯ能明显改善肺通气功能，作为吸入性损伤的综合治疗，吸入ＮＯ疗法值得进一步研究。     

一氧化氮对吸入性损伤犬肺功能的改善作用及机制

目的：评价吸入一氧化氮（ＮＯ）对烟雾吸入性损伤犬肺功能的改善效果，并验证其作用机制。方法：２１只犬随机分为３组，烟雾吸入后的对照组（８只）给予单纯吸氧（ＦｉＯ２０．４５）；治疗组（９只）吸氧（ＦｉＯ２０．４５）＋０．００４５％ＮＯ，连续监测１２小时血气变化；正常组（４只）不致伤，用于建立组织学对照。数据行多个样本均数间方差分析。结果：治疗组肺氧合功能明显改善（Ｐ均＜０．０５），肺通气功能也明显改善（Ｐ均＜０．０５）；动脉血和肺组织环磷酸鸟苷（ｃＧＭＰ）明显升高（Ｐ均＜０．０１）。结论：吸入ＮＯ能明显改善肺功能，其作用机制为提高平滑肌细胞内ｃＧＭＰ水平。推荐临床应用吸入ＮＯ作为吸入性损伤的综合治疗方法。     

吸入一氧化氮对犬烟雾吸入性损伤血液流变学的影响

目的评价犬烟雾吸入性损伤吸入一氧化氮（ＮＯ）对血液流变学的影响。方法１７只犬随机分二组，烟雾吸入后，对照组（ｎ＝８）单纯吸氧（ＦｉＯ２，０４５），治疗组（ｎ＝９）吸氧（ＦｉＯ２，０４５）＋０００４５％ＮＯ，连续监测血液流变学有关参数，数据行多个样本均数间方差分析和相关分析。结果治疗组ＲＢＣ数和ＲＢＣ压积（Ｈｃｔ）比对照组显著降低（Ｐ＜００５）；ＲＢＣ聚集指数（ＥＡＩ）比对照组降低而ＲＢＣ刚性指数（ＥＲＩ）则升高（Ｐ＜００５～００１）；低切全血粘度（Ｌηｂ）、全血还原粘度（Ｌηｈ）和血浆粘度（ηＰ），治疗组比对照组明显降低（Ｐ＜００５～００１）；治疗组ＮＯ含量升高与ＥＡＩ、Ｌηｈ和ηＰ降低呈显著负相关（ｒ值分别为－０９４，－０９５，－０９３，Ｐ均＜００１）。结论吸入性损伤后血液粘度也有不同程度升高，吸入ＮＯ有不同程度降低吸入性损伤血液的高凝趋势，值得进一步研究     

一氧化氮吸入疗法对烟雾吸入性损伤犬心脏能量代谢和病理变化的研究

目的：评价烟雾吸入性损伤犬吸入一氧化氮（ＮＯ）后心脏病理改变与心室肌组织能量代谢的变化。方法：２１只犬随机分为３组,烟雾吸入损伤后,对照组（８只）单纯吸氧（ＦｉＯ２＝０．４５）,治疗组（９只）吸氧（ＦｉＯ２＝０．４５）＋０．００４５％ＮＯ,正常组（４只）不致伤,用于病理和组织学对照。实验终点进行心室肌组织学和病理形态学检测。结果：对照组ＡＴＰ含量和能量负荷（ＥＣ）显著低于正常组和治疗组（Ｐ均＜０．０１）,对照组ＡＤＰ和ＡＭＰ含量明显低于正常组（Ｐ均＜０．０１）,但ＡＤＰ明显高于治疗组（Ｐ＜０．０５）;心脏光镜和电镜病理所见,治疗组病理性改变程度较对照组轻。结论：在烟雾吸入性损伤犬模型中,吸入ＮＯ可不同程度改善心肌组织能量代谢,心脏病理形态改变也有一定程度减轻,表明ＮＯ吸入疗法对改善心脏能量代谢和病理改变有益。     

吸入一氧化氮治疗兔油酸急性呼吸窘迫综合征

目的：探讨吸入一氧化氮（ＮＯ）对急性呼吸窘迫综合征（ＡＲＤＳ）肺换气功能的影响及其毒副作用。方法：油酸诱发新西兰兔ＡＲＤＳ模型后分组（ｎ＝９）进行机械通气治疗４ｈｒ：（１）对照组；（２）吸入２０ｐｐｍＮＯ（ＮＯ组）。于动物实验的基础状态、治疗前测定ＰａＯ２／ＦｉＯ２、肺内静动脉分流（Ｑ·ｓ／Ｑ·ｔ）、血ＮＯ２－／ＮＯ３－和高铁血红蛋白（ＭｅｔＨｂ），治疗后ＰａＯ２／ＦｉＯ２于１、２、４ｈｒ，其余指标于４ｈｒ复查一次。观察肺病理并测定肺湿干重比（Ｗ／Ｄ）。结果：治疗后，对照组ＰａＯ２／ＦｉＯ２较治疗前呈下降趋势（４ｈｒ，Ｐ＜０．０５），Ｑ·ｓ／Ｑ·ｔ增加（４ｈｒ，Ｐ＜０．０１），ＮＯ组各时点ＰａＯ２／ＦｉＯ２均较治疗前和同时点的对照组明显增加（Ｐ＜０．０１～０．０５），Ｑ·ｓ／Ｑ·ｔ明显低于治疗前和同时点的对照组（４ｈｒ，Ｐ＜０．０５，Ｐ＜０．０１）。实验结束时，ＮＯ组ＮＯ２－／ＮＯ３－和ＭｅｔＨｂ较对照组显著增加（Ｐ＜０．０５，Ｐ＜０．０１），两组的肺病理和Ｗ／Ｄ无明显区别。结论：吸入２０ｐｐｍ能够明显改善兔油酸型ＡＲＤＳ的肺换气功能，无明显近期毒副作用     

吸入小剂量一氧化氮降低先天性心脏病肺动脉高压的初步研究

目的：探索吸入小剂量一氧化氮（ＮＯ）对先天性心脏病（先心病）肺动脉高压的治疗作用。方法：先心病合并肺动脉高压〔平均肺动脉压（ＭＰＡＰ）＞６．４ｋＰａ（１ｋＰａ＝７．５ｍｍＨｇ）〕患者９例，年龄３～２０岁，在自主呼吸下吸入３６±１０ｖｐｍ的ＮＯ，监测并记录ＮＯ吸入前和吸入后１、３、５、１０和１５分钟时的ＭＰＡＰ、平均血压（ＭＢＰ）、心率（ＨＲ）、脉搏氧饱和度（ＳｐＯ２）、混合静脉血氧饱和度（ＳｖＯ２）等参数的变化。结果：基础ＭＰＡＰ为９．５±１．８ｋＰａ，吸入ＮＯ后各时间点ＭＰＡＰ显著降低，波动于８．９～８．１ｋＰａ（Ｐ＜０．０５）；并可明显增高ＳｖＯ２（Ｐ＜０．０５），从０．７６±０．０６升至０．８３±０．０２（Ｐ＜０．０５）；ＭＢＰ、ＨＲ和ＳｐＯ２无明显变化。结论：吸入小剂量ＮＯ确能选择性降低先心病合并肺动脉高压患者的肺动脉压，并增高ＳｖＯ２；吸入小剂量ＮＯ对这类患者围手术期有显著治疗前景。     

一氧化氮吸入疗法对烟雾吸入性损伤犬心脏能量代谢和病 …

目的：评价烟雾吸入性损伤犬吸入一氧化氮后心脏病理与心室肌组织能量代谢的变化。方法：２１只犬随机分为３组,烟雾吸入损伤后,对照组单纯吸氧,治疗组吸氧（ＦｉＯ２＝０．４５）＋０００４５％ＮＯ,正常组不致伤,用于病理和组织学对照。实验终点进行心室肌组织学和病理形态学检测。     

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。     

Efficiency of inhaled nitric oxide as rescue therapy during severe ARDS: Survival and factors associated with the first response

PURPOSE: The purpose of this study was to determine if the response to inhaled nitric oxide (NO) as salvage therapy is an independent factor for survival in adult respiratory distress syndrome (ARDS) patients and to identify the factors that predict the response to inhaled NO during ARDS. MATERIALS AND METHODS: This was a multicenter, 2-year retrospective, clinical study in five university surgical or medical intensive care units, including all consecutive patients with ARDS in whom inhaled NO was tried. Clinical data (medical history, diagnoses), general severity scores (SAPS II, OSF), biological data, radiological and hemodynamic data at admission, at the beginning of the ARDS, and under treatment with inhaled NO were recorded. The NO response was defined as the variation of PaO2/Fio2 ratio before initiation and after 30 minutes of NO inhalation (VarPaO2/FiO2). RESULTS: Ninety-three patients aged 49 +/- 18 years were studied. Mean SAPS II was 45 +/- 16. Before the beginning of inhaled NO, PaO2/Fio2 ratio was 95 +/- 53 mm Hg and lung injury score 2.7 + 0.3. VarPao2/Fio2 when NO was started (11 +/- 4 ppm) was 26 +/- 44.5 mm Hg (median 17 mm Hg). Intensive care unit mortality was 74%. None of the parameters studied were predictors of response to inhaled NO, although there was a tendency for the youngest patients with the more severe hypoxemia to have a better response. Response to first inhaled NO test (VarPaO2/FiO2) was univariately associated with survival (Survivors: 45 +/- 44 mm Hg vs. Nonsurvivors: 20 +/- 43 mm Hg, P = .01), but this difference disappeared after adjusting for other prognostic factors (P = .16) selected by multivariate analysis. Finally, inhaled NO was continued for more than 1 day for 75 patients, and definitively stopped for 18 patients. Intensive care unit mortality (73% vs. 78%) was not different between these groups (P = .25, Log-rank test). CONCLUSIONS: We conclude that (1) efficacy of inhaled NO in improving oxygenation was moderate and difficult to predict, (2) response to first NO inhalation was not associated with prognosis, and (3) treatment of the most severe ARDS patients with inhaled NO did not influenced their intensive care unit survival.     

吸入一氧化氮对大鼠肝脏毒副作用的影响

目的　评价吸入外源性一氧化氮 (NO)对正常大鼠肝脏的毒副作用。方法　 72只大鼠随机分为三组 :吸氧组 (G1)单纯吸氧 (FiO2 0 .40 ) ;低浓度NO吸入组 (G2 )和高浓度NO吸入组 (G3 )除吸氧外 ,分别吸入 40 ppm和 80 ppm的NO ,分别于 2、8、12、2 4小时取标本检测 ;另取 6只大鼠做正常值和组织学对照。数据行多个样本均数间方差分析。结果　肝组织含水量三组间无明显差异 (P >0 .0 5 ) ,三组呼出气NO2 浓度G3 比G1和G2 和正常值显著升高 (P <0 .0 1) ,G3 GPT2 4小时明显高于G1(P <0 .0 1)、G2 和正常值 (P <0 .0 5 ) ,G2 TBil2 4小时明显低于G1和G3 ,G3 MHB分别高于G1和G2(P <0 .0 5、P >0 .0 5 ) ,G1和G3 均可见到组织形态学改变 ,G2 组改变则较轻。结论　吸入低浓度NO无明显毒副作用 ,而吸入高浓度NO对肝组织可能有一定的损伤     

Inhaled nitric oxide in acute respiratory distress syndrome with and without septic shock requiring norepinephrine administration: a dose–response study

BACKGROUND: The aim of this prospective study was to assess whether the presence of septic shock could influence the dose response to inhaled nitric oxide (NO) in NO-responding patients with adult respiratory distress syndrome (ARDS). RESULTS: Eight patients with ARDS and without septic shock (PaO2 = 95 +/- 16 mmHg, PEEP = 0, FiO2 = 1.0), and eight patients with ARDS and septic shock (PaO2 = 88 +/- 11 mmHg, PEEP = 0, FiO2 = 1.0) receiving exclusively norepinephrine were studied. All responded to 15 ppm inhaled NO with an increase in PaO2 of at least 40 mmHg, at FiO2 1.0 and PEEP 10 cmH2O. Inspiratory intratracheal NO concentrations were recorded continuously using a fast response time chemiluminescence apparatus. Seven inspiratory NO concentrations were randomly administered: 0.15, 0.45, 1.5, 4.5, 15, 45 and 150 ppm. In both groups, NO induced a dose-dependent decrease in mean pulmonary artery pressure (MPAP), pulmonary vascular resistance index (PVRI), and venous admixture (QVA/QT), and a dose-dependent increase in PaO2/FiO2 (P 相似文献   

Methemoglobin formation in children with congenital heart disease treated with inhaled nitric oxide after cardiac surgery

OBJECTIVE: Inhaled nitric oxide (NO) is used as a therapy of pulmonary hypertension in children after cardiac surgery. Hemoglobin binds to NO with great affinity and forms methemoglobin by oxidation in the erythrocyte. Once produced, methemoglobin is unable to transport and unload oxygen in the tissues. The amount of available hemoglobin in the body for oxygen transport is thereby reduced. Anemia, acidosis, respiratory compromise and cardiac disease may render patients more susceptible than expected for a given methemoglobin level. The goal of the present study was to review the cumulative effect of inhaled NO on methemoglobin formation in critically ill children. We therefore looked for methemoglobin levels in children with congenital heart disease after cardiac surgery who were treated with inhaled NO in a range of 5-40 ppm. METHODS: We retrospectively reviewed the medical charts of 38 children with congenital heart disease after cardiac surgery. We extracted demographic data and physiological measurements at the following time points: (1) T0 = before starting inhaled NO therapy, (2) T1 = 24 h after the beginning of inhaled NO therapy, (3) T2 = half-time therapy, (4) T3 = end of therapy, (5) T4 = 24 h after finishing inhaled NO therapy. RESULTS: The median duration of inhaled NO therapy was 5.5 days (interquartile range 6, range 2-29), NO concentrations at T1 and T2 were 16 ppm (10, 5-40) and 12.5 ppm (12.3, 2-40), respectively. The median cumulative dose of inhaled NO was 1699 ppm (2313, 193-7018). Methemoglobin levels increased moderately, but significantly, during therapy ( T0 vs T1 p<0.05 and T0 vs T2 p<0.001). The highest methemoglobin level measured was 3.9%. Methemoglobin levels correlated positively with the inhaled NO doses applied at T1 ( r(2)=0.8376; p<0.01) and at T2 ( r(2)=0.8945; p<0.01). At T1 the methemoglobin level correlated negatively with the T1 blood pH value. The overall mortality rate was 13.2% (5 of 38 study patients died). There was no significant difference in methemoglobin levels between survivors and non-survivors. CONCLUSION: We conclude from our data that the use of inhaled NO therapy for children with congenital heart disease after cardiac surgery in the described range of 5-40 ppm, resulting in a maximum of 4% methemoglobin blood level, is feasible and safe. However, we recommend the use of the minimal effective dose of inhaled NO and continuous monitoring of methemoglobin levels, especially in cases of anemia or sepsis in critically ill children.     

氦-氧混合气体治疗重症慢性阻塞性肺病

目的：探讨吸入氦－氧混合气对重症慢性阻塞性肺病（COPD）机械通气患者的治疗作用以及对机械通气患者脱机的作用。方法：选择12例重症COPD机械通气患者随机分为氦－氧混合气组（70％氦；30％氧）和对照组（FiO2:30%),观察治疗前、治疗后30、90min、6h的呼吸力学指标（气道峰压、平台压、吸气阻力、呼气阻力）以及内源性呼气末正压的变化；选择准备脱机的机械通气患者6例，按自身对照方式脱机后随机先后吸入氦－氧混合气，（70％氦－30％氧）和低浓度氧（FiO2:30%)观察治疗前、治疗后30、90min、6h和停止治疗后30min(重新上机进行压力支持通气）的动脉血气指标。结果：机械通气患者应用氦氧混合气治疗后气道压力、气道阻力和内源性呼气末正压均有明显下降，与对照组比较差异有显著性意义；脱机患者吸入氦－氧混合气后与对照组比较pH、PaO2、PaCO2差异均具有显著性意义。结论：吸入氦－氧混合气在治疗重症COPD机械通气患者方面能够明显降低气道压力和气道阻力，避免气压伤的发生；应用氦氧混合气可以有效避免脱机患者血气指标的恶化，可以有助于患者的顺利脱机。     

Aerosol delivery of diethylenetriamine/nitric oxide, a nitric oxide adduct, causes selective pulmonary vasodilation in perinatal lambs.

Postnatal adaptation of the pulmonary circulation is mediated partly by endothelium-derived nitric oxide (NO). Recent studies have demonstrated that inhaled NO causes selective and sustained vasodilation in infants with persistent pulmonary hypertension of the newborn. Because the short half-life of NO limits its clinical application, we hypothesized that aerosol delivery of an NO-adduct, diethylenetriamine (DETANO), can cause sustained and selective pulmonary vasodilation. To test the acute effects of DETANO, we studied the pulmonary vascular response of late-gestation fetal lambs (n = 8; age = 138 days; term = 147) to aerosolized DETANO in the presence of an endothelium-derived NO inhibitor, nitro-L-arginine. To determine whether DETANO has a sustained effect, fetal lambs were ventilated with FiO2 0.10 before and 15 minutes after they were treated with aerosolized DETANO. Fetal lambs were acutely prepared. Nitro-L-arginine (1 mg/min x 30 minutes) was infused into the left pulmonary artery before ventilation with FiO2 1.00 for 30 minutes, followed by continued ventilation with FiO2 0.10 for 10 minutes. This represented the control period. Ventilation was continued with FiO2 1.00, and aerosolized DETANO was given in doses of 0.1, 0.4, and 1.0 mg. Fifteen minutes after the last dose of DETANO was administered, animals were ventilated with FiO2 0.10. In the control period, during ventilation with FiO2 0.10, left pulmonary artery flow was 122+/-33 mL/min and decreased to 104+/-22 mL/min. Aerosol delivery of DETANO increased left pulmonary artery flow to 176+/-26 mL/min (P<.05) and had no effect on aortic pressure or heart rate. After DETANO was administered, ventilation with FiO2 0.10 did not cause any change in left pulmonary artery flow. We conclude that DETANO can cause selective fetal pulmonary vasodilation. Aerosol delivery of DETANO may increase the clinical applications of NO.     

一氧化氮与内皮素-1对慢性缺氧性肺动脉高压的影响

目的 为探讨一氧化氮(NO)和内皮素-1(ET—1)与慢性缺氧肺动脉高压的关系以及吸入NO和吸入氧的治疗效果。方法 实验时将动物(大鼠)随机分成对照组(组1)、缺氧组(组2)、缺氧加吸氧组(组3)、缺氧加NO吸入组(组4)和缺氧加NO吸入加氧吸入组(组5)。结果 组2与组1比较平均肺动脉压明显增高,氧分压、血浆NO明显降低,血浆ET—1明显增高。析因分析处理间P<0.01,交互影响P<0.01,表明吸入NO同时吸氧有交互影响。结论NO与ET—1参与了慢性缺氧肺动脉高压的形成,吸入NO的同时吸氧能显著降低慢性缺氧性肺动脉高压,增强肺氧合。