肠系膜淋巴管结扎对失血性休克大鼠肺组织一氧化氮及其表达的影响

目的 观察结扎肠系膜淋巴管对不同时期重症失血性休克大鼠肺组织一氧化氮（NO）及其表达的影响，探讨肠淋巴途径在休克大鼠急性肺损伤（ALI）中的作用。方法 雄性Wistar大鼠78只，按随机数字表法分为假手术组（n=6）、休克组（n=42）和结扎组（n=30）。休克组与结扎组复制重症失血性休克模型，结扎组于休克复苏后行肠系膜淋巴管结扎术；休克组于休克后90min、输液复苏后0h，休克组及结扎组于输液复苏后1、3、6、12和24h各时间点处死大鼠，制备肺组织匀浆，检测NO及其合酶的变化；用逆转录-聚合酶链反应（RT—PCR）测定各组大鼠肺组织诱生型一氧化氮合酶（iNOS）．mRNA表达。结果 休克组大鼠复苏后3h肺组织NO含量、NOS活性及iNOSmRNA表达开始升高，复苏后6～12h持续在较高水平，均显著高于假手术组、休克后90min及复苏后0h（P〈0．05或P〈0．01）；结扎组仅于3h和6h增高，且结扎组复苏后6、12和24h肺组织NO含量、NOS活性以及iNOSmRNA表达均显著低于休克组相同时间点（P〈0．05或P〈0．01）。结论 肠系膜淋巴管结扎可降低重症失血性休克大鼠肺组织NO生成及iNOSmRNA表达，从而减轻肺损伤。     

Improvement of portal hypertension and hepatic blood flow in cirrhotic rats by oestrogen

BACKGROUND: In this study, we investigated the effects of oestrogen on nitric oxide synthase activity and nitric oxide production using the cirrhotic rat liver. MATERIAL AND METHODS: Cirrhosis was induced by dimethylnitrosamine. Estradiol valerate was subcutaneously injected twice at week 4 after dimethylnitrosamine treatment. Furthermore, subcutaneous injection of an oestrogen receptor antagonist, ICI-182.780, was performed 2 days before administration of estradiol valerate. Portal pressure and hepatic blood flow were measured. Nitric oxide synthase activity was assessed by l-citrulline generation. Sinusoidal endothelial cells were isolated from the cirrhotic rat liver and cultured. The cells were incubated with estradiol and/or ICI-182.780 for 24 h. Images for nitric oxide in sinusoidal endothelial cells were obtained using diaminofluorescein-2 diacetate. RESULTS: Cirrhotic rats treated with estradiol valerate showed a significant decrease in portal pressure and a significant increase in hepatic blood flow compared with those of control cirrhosis rats. However, in cirrhotic rats treated with ICI-182.780, the reduction of portal pressure and elevation of hepatic blood flow were completely inhibited. In cirrhotic rats treated with estradiol valerate, nitric oxide synthase activity was increased compared with that in control cirrhotic rats. The fluorescent level of intracellular nitric oxide in estradiol-stimulated, cultured, sinusoidal endothelial cells was higher than that in nontreated sinusoidal endothelial cells. CONCLUSIONS: The present study indicated that oestrogen plays an important role in the enhancement of nitric oxide production in sinusoidal endothelial cells of cirrhotic liver and reduces the portal pressure in cirrhotic rats.     

氯沙坦对肝硬化大鼠血清内毒素及一氧化氮的影响

目的：探讨氯沙坦对肝硬化大鼠血清一氧化氮（NO）、内毒素水平的影响。方法：成年雄性Wistar大鼠肝硬化形成后，随机分为两组，即模型组、氯沙坦治疗组，另取6只正常大鼠作为正常组。治疗21d，采取硝酸还原酶法测量血清NO水平、鲎试剂偶氮显色法测量内毒素水平。结果：与正常组大鼠相比，模型组大鼠血清NO与内毒素水平显著增高。治疗组与模型组相比，上述指标降低具有显著性。结论：氯沙坦可降低肝硬化大鼠血清NO、内毒素水平。     

雾化吸入氯胺酮对哮喘大鼠肺组织一氧化氮及一氧化氮合酶的影响

目的通过建立大鼠支气管哮喘模型,观察不同浓度氯胺酮对哮喘大鼠肺组织iNOS活性及NO含量的影响。方法SD大鼠随机分成对照组(N组)、哮喘模型组(A组)、不同浓度氯胺酮预处理组(分别为K1组、K2组)和地塞米松组(D组),每组8只。A组大鼠用卵白蛋白辅以百日咳杆菌菌苗和氢氧化铝为佐剂注射致敏,2周后雾化吸入卵蛋白激发哮喘;氯胺酮处理组大鼠用同样方法致敏,但在激发前分别给予雾化吸入氯胺酮25 g/L(K1组)和50 g/L(K2组);D组在激发前给予雾化吸入0.01%地塞米松;N组用生理盐水替代卵蛋白进行注射和吸入。每组分别测定其肺组织NO2-/NO3-水平、肺组织诱导型NOS(iNOS)和原生型NOS(cNOS)活性水平,并用免疫组织化学法观察iNOS在大鼠哮喘模型肺组织中的分布。结果A组肺组织中NO2-/NO3-和iNOS水平升高,iNOS和肺组织NO2-/NO3-水平呈高度正相关;K1、K2组肺组织中NO2-/NO3-和iNOS水平低于A组(P<0.05);D组肺组织中NO2-/NO3-和iNOS水平亦低于A组(P<0.05)。结论25 g/L或50 g/L的氯胺酮雾化吸入可抑制哮喘大鼠肺组织iNOS活性,降低NO含量,减轻大鼠肺部炎症。     

Vasodilator responses to nitric oxide are enhanced in mesenteric arteries of portal hypertensive rats

Abstract. Nitric oxide (NO) is discussed as a mediator of the splanchnic hyperaemia in portal hypertension. We assessed the vasorelaxation by the NO-dependent vasodilator acetylcholine, the NO donor 3-morpholino-sydnonimine (SIN-1) and forskolin, a stimulator of the adenylate cyclase pathway in potassium-preconstricted isolated perfused mesenteric arteries of portal vein-ligated and sham-operated rats. Dilator responses to acetylcholine and SIN-1 were significantly enhanced in vessels of portal vein-ligated rats as compared to sham-operated rats, whereas no difference was found in forskolin-induced vasodilatation. This suggests enhanced reactivity of the vasculature to NO in experimental portal hypertension.     

The role of the interaction between endogenous opioids and nitric oxide in the pathophysiology of ethanol-induced gastric damage in cholestatic rats

Interaction between endogenous opioids and nitric oxide (NO) has been shown in different biological models and pharmacological evidence suggest that opioids can induce NO release in endothelium as well as in neural cells. Cholestasis is associated with NO overproduction. The reason for increased NO synthesis is not clearly known but it can potentiate development of gastric mucosal damage in cholestatic subjects. Based on increased plasma levels of endogenous opioids and existence of NO overproduction in cholestasis, the present experiments were performed to investigate the role of interaction between endogenous opioids and NO in generation of ethanol-induced gastric damage in cholestatic rats. Cholestasis was induced by surgical ligation of bile duct and sham-operated rats served as controls. The animals received either 20 mg/kg of naltrexone or saline for 6 days and then were fasted and received L-arginine (200 mg/kg), NG-nitro-L-arginine methylester (L-NAME; 2, 5 and 10 mg/kg) or saline. The ethanol-induced gastric mucosal damage was significantly more severe in cholestatic rats than in sham-operated animals (115 +/- 12 mm2 vs. 72 +/- 11 mm2, P < 0.05). L-NAME significantly enhanced the development of gastric mucosal lesions in sham-operated rats. But in cholestatic animals, L-NAME decreased and L-arginine enhanced the severity of gastric damage. Pretreatment of animals with naltrexone decreased severity of gastric mucosal damage in cholestatic rats. Concurrent administration of naltrexone with L-arginine was protective against ethanol-induced gastric damage in both normal and cholestatic groups. Administration of naltrexone with L-NAME had the same effect in cholestatic and control rats and increased severity of gastric damage. Plasma levels of NO2- + NO3- were significantly higher in cholestatic rats than control animals (72 +/- 6 microM vs. 39 +/- 3 microM, P < 0.05). Pretreatment of animals with naltrexone significantly reduced plasma levels of NO2- + NO3- in cholestatic animals, but not in control rats (33 +/- 6 microM vs. 32 +/- 4 microM). The protective effect of L-NAME against gastric damage in cholestatic rats can be explained by inhibition of NO overproduction and it seems that interaction between opioids and NO may have an important role in generation of NO overproduction and gastric complications in cholestatic rats.     

On the relation of nitric oxide to nifedipine-induced gingival hyperplasia and impaired submandibular glands function in rats in vivo

Calcium-channel blockers such as nifedipine could be associated with gingival overgrowth. The aim of this study was to examine the role of nitric oxide (NO) on nifedipine-induced gingival hyperplasia along with submandibular secretory function in rats. Animals in divided groups received nifedipine (250 mg/kg diet) alone and in combination with L-arginine (2.25% w/v) or N(omega)-nitro-L-arginine methyl ester (L-NAME) (0.7% w/v) in drinking water for 20 days. Controls received only tap water. Pure submandibular saliva was collected intraorally by micropolyethylene cannula and the mandibular gingiva was examined by means of dissecting microscope for signs of redness, thickness, inflammation and exuda. Twenty-day nifedipine treatment induced gingival hyperplasia accompanied with reduced salivary flow rate and concentrations of total protein, epidermal growth factor (EGF) and calcium in comparison with controls. Co-treatment of animals with nifedipine and L-arginine protected from gingival hyperplasia and retained flow rate, and concentrations of total protein, EGF and calcium in normal levels. Co-treatment of animals with nifedipine and L-NAME potentiated nifedipine-induced gingival hyperplasia and reductions in flow rate and concentrations of total protein, EGF, and calcium. It is concluded that nifedipine-induced gingival hyperplasia is associated with salivary dysfunction. Activation of cGMP-dependent positive signal-transduction mechanisms in salivary glands might be the mechanism for protective effects of NO against nifedipine-induced gingival hyperplasia.     

慢性乙型肝炎患者血浆内皮素、一氧化氮、心钠素、降钙素基因相关肽的变化及意义

目的　探讨慢性乙型肝炎、肝炎肝硬化患者血浆内皮素 (ET)、一氧化氮 (NO)、心钠素 (ANP)、降钙素基因相关肽 (CGRP)的变化及相互关系。方法　对 60例慢性乙型肝炎、3 0例肝炎肝硬化患者 ,采用放射免疫法测定治疗前后ET、ANP、CGRP ,硝酸还原酶法测定NO并作相关分析 ,肝硬化患者同时测定门静脉内径及血流量。结果　①慢性乙型肝炎、肝硬化患者血浆ET、NO明显高于正常对照组 ,均P <0 .0 5 ,且随着病变的加重 ,两者升高得更显著 ,CGRP水平明显低于正常对照组 ,P <0 .0 1;ANP与对照组无差别 ,P >0 .0 5。②慢性乙肝组肝功能好转 ,ET、ANP、CGRP无显著性变化 ,P >0 .0 5 ,肝硬化组肝功能好转 ,ET下降 ,P <0 .0 1,CGRP上升 ,P <0 .0 5。慢乙肝重度、肝硬化组治疗后NO下降 ,P <0 .0 5 ,P <0 .0 1。③直线相关分析表明 ,ET与NO呈正相关 ,P <0 .0 1;ET、NO、ANP、CGRP与肝功能无密切关系。结论　血管活性因子ET、NO、ANP、CGRP共同参与了慢性乙型肝炎的发生发展过程     

Warming and response to contractile agents in calf cardiac vein: role of the nitric oxide

The effects of warming on the response to various contractile agents of calf cardiac vein were studied using 2.5-mm long cylindrical segments. Concentration-response curves for carbachol (10(-9)-3 x 10(-4) m), 5-hydroxytryptamine (5-HT; 10(-8)-3 x 10(-3)), potassium chloride (KCl; 10(-4)-5 x 10(-2) m) and calcium chloride (CaCl2; 10(-4)-10(-2)) were isometrically recorded at 37 and 41 degrees C (warming). During warming the sensitivity, but not the maximal response, of carbachol 5-HT, KCl, and CaCl2 was significantly higher than at 37 degrees C. Warming to 41 degrees C after treatment with NG-nitro-L arginine methyl esther (10(-5) m) did not modify the effect of warming. These results suggest that nitric oxide seems to have no role in the warming-induced responses in calf cardiac vein.     

内皮素和一氧化氮在烧伤后肝脏血流调节中的作用

目的：研究内皮素（ＥＴ）和一氧化氮（ＮＯ）在烧伤后肝脏血流调节中的作用。方法：动态观察大鼠３０％Ⅲ度烧伤后血浆及肝脏ＥＴ、ＮＯ含量及肝脏血流量的变化,应用ＥＴ受体拮抗剂和外源性ＮＯ载体观察其对烧伤大鼠肝脏血流量的影响。结果：大鼠烧伤后肝脏血流量明显下降,伤后血浆及肝组织ＥＴ和ＮＯ含量明显升高,由于ＥＴ升高幅度相对较大,ＥＴ／ＮＯ比值也显著增加,肝组织ＥＴ、ＥＴ／ＮＯ改变与肝脏血流量的降低呈显著负相关;伤后在一定的液体复苏下应用两种ＥＴ受体拮抗剂和ＮＯ供体在一定程度上明显使肝血流量增加,同时拮抗ＥＴ受体Ａ（ＥＴＡ）、ＥＴ受体Ｂ（ＥＴＢ）较单独拮抗ＥＴＡ效果好,ＥＴ受体拮抗剂和ＮＯ供体配合使用效果更佳。结论：烧伤后由于肝脏ＥＴ的增加和内源性ＮＯ相对不足,导致肝脏血管收缩造成肝脏血流量下降,拮抗ＥＴ的作用和（或）补充外源性ＮＯ则可一定程度逆转烧伤后肝脏血流量下降     

大鼠脑缺血再灌注损伤后血浆内皮素、一氧化氮含量变化及通心络对其影响

目的：探讨大鼠脑缺血再灌注损伤后血浆一氧化氮（NO）、内皮素（ET）含量变化及通心络对其的作用。方法：采用大鼠MCAO模型，应用放免方法观察缺血后第3、5、14及30d NO、ET含量变化。结果：MCAO后血浆ET浓度显著升高（P〈0．05），而NO浓度显著下降（P〈0．05）；通心络能升高血浆NO浓度，降低ET浓度。结论：MCAO缺血损伤时，NO、ET起着重要作用，通心络则具有防治脑缺血性损害的作用。     

神经生长因子对急性脑梗死大鼠神经功能和一氧化氮合酶含量的影响

目的 观察神经生长因子（NGF）对实验性急性脑梗死大鼠的疗效，初步探讨可能的机制。方法 将24只制备成的脑梗死模型大鼠随机分为3组，分别用神经生长因子（NGF）、胞磷胆碱钠（CS）和生理盐水（NS）治疗，于治疗前后检查动物的神经病学评分改变；再将55只大鼠随机分为实验组（25只）、对照组（25只）和正常组（5只），实验组急性脑梗死后即刻肌肉注射NGF，对照组注射等量NS。对照组和实验组大鼠分别在脑梗死后1h、3h、6h、12h、24h断头取脑，检测脑组织中一氧化氮合酶（NOS）含量。结果 与治疗前比较，NGF组和CS组大鼠治疗后神经病学评分均低于NS组（P〈0．05）；脑梗死大鼠梗死区脑组织中NOS活性在梗死后1h、3h较正常组明显升高（P〈0．01）；实验组大鼠NOS含量在脑梗死后1h、3h、6h较对照组明显下降（P〈0．01）。结论 NGF可明显促进急性脑梗死大鼠神经功能的恢复，机制之一可能是通过抑制急性脑梗死后NOS的活性起到保护损伤脑神经元的作用。     

Bioactivation of nitroglycerin to nitric oxide (NO) and S-nitrosothiols in the rat liver and evaluation of the coexisting hypotensive effect

The aim of the present study was to investigate nitroglycerin (NTG) bioactivation pathways in the liver after various periods of its administration. We also attempted to elucidate the relationship between nitric oxide (NO) and S-nitrosothiol (SNT) levels, and concentration of nonprotein thiols (NPSH) and intensity of peroxidative processes. Intravenous injections of NTG cause an increase in NO and SNT levels in the rat liver. The same intravenous NTG injections in the rats pretreated with 5-day i.p. NTG administrations lead to a drop in the levels of the biologically active NO, SNT and NPSH, with no concomitant changes in the rate of lipid peroxidation. This indicates that after such period of nitroglycerin pretreatment, levels of pharmacologically active NO and SNT decrease. However, during longer periods of NTG administration (for 10 and 17 days) NO, SNT and NPSH concentrations remain at the control level in spite of a considerably enhanced lipid peroxidation, which indicates that tolerance did not develop. Effects of NTG bioactivation in the liver, i.e. the levels of NO and SNT released from it, after different periods of drug administration correspond with hypotensive effects, which are known to be dependent on NTG biodegradation in vascular endothelial cells. The changes in NO and SNT levels observed in the rat liver after different periods of NTG administration parallel alterations in the hypotensive effect. In conclusion, NTG treatment for 10 and 17 days does not lead to tolerance, however, a transient loss of its pharmacological activity occurs after 5-day NTG pretreatment.     

正心泰对急性心肌梗死家兔心肌及血管内皮细胞一氧化氮合酶、内皮素基因表达的影响

目的:观察正心泰对急性心肌梗死(AMI)家兔心肌及血管内皮细胞一氧化氮合酶(NOS)和内皮素(ET)的影响.方法:将40只家兔随机分为假手术组、模型组、卡托普利组、正心泰高剂量和低剂量组5组,给药后1周,通过结扎冠状动脉前降支方法,造成AMI模型.制模后3 h处死动物,取心肌组织制成切片,应用原位杂交及图像分析仪方法进行内皮型一氧化氮合酶(eNOS)mRNA和ET-1 mRNA表达的分析.结果:正心泰高、低剂量组及卡托普利组的eNOS mRNA表达均较模型组提高,ET-1 mRNA表达则均有所下降,相比较均有显著性差异(P<0.05或P<0.01).结论:正心泰与卡托普利一样通过调控NOS和ET基因表达来达到对AMI的治疗作用.     

冷应激溃疡大鼠下丘脑和肾上腺一氧化氮合成酶2与内皮素-1表达及针刺保护机制的研究

目的观察针刺足三里穴对急性胃溃疡的保护效应，并探讨其作用机理。方法将SD雄性大鼠随机分为正常对照组、单纯应激组、针刺预防应激组，应用胃粘膜溃疡指数的计算和RT-PCR的方法研究针刺足三里对大鼠的冷应激性溃疡的保护和下丘脑及肾上腺一氧化氮合成酶(NOS)2和内皮素(ET)-1的表达情况，经图像分析系统照相并进行半定量。结果针刺足三里穴可以明显减少冷应激造成的溃疡指数。下丘脑NOS2和ET-1均参与了冷应激溃疡病理过程，针刺足三里穴可以下调其表达。在应激过程中，肾上腺中并无NOS2和ET-1的病理性表达。结论针刺对冷应激溃疡具有保护作用，该种保护作用是通过对抑制下丘脑NOS2和ET-1的病理性表达来实现的，NOS2和ET-1在肾上腺中不参与应激过程。     

沙漠干热环境创伤失血性休克大鼠继发性肺损伤时一氧化氮合酶等变化研究

目的 研究沙漠干热环境中创伤失血性休克大鼠肺脏发生继发性损伤时,肺组织病理改变与肺组织一氧化氮(NO)浓度、诱导型一氧化氮合酶(iNOS) mRNA表达量的变化.方法 在兰州军区乌鲁木齐总医院动物实验科“西北特殊环境人工实验舱”中,140只雄性SD大鼠随机(随机数字法)分为常规环境创伤失血性休克组(常温组)和干热环境创伤失血性休克组(干热组),每组又分别设对照组、休克后0、0.5、1、1.5、2、3h组7个亚组,每组10只.对照组不做处理,干热组预热60 min,麻醉、固定,使用静脉留置针行右颈动、静脉和右股动脉插管,稳定10 min后,利用2500 g铁轮于30 cm高度击中SD大鼠左下肢股骨中上段造成粉碎性骨折,致伤后简易包扎伤口,经右股动脉放血使MAP维持在(35 ±5) mmHg(1 mmHg =0.133 kPa),继续监测60 min后进行复苏.成功建立创伤失血性休克模型后,依据分组相应时间点,打开胸腔,留取肺灌洗液、肺组织,常温组除预热外其余操作相同.HE染色观察肺组织病理学改变和一步法检测肺组织NO质量摩尔浓度,荧光定量PCR检测iNOS mRNA表达量的变化.对计量资料进行t检验与单因素方差分析,各指标间进行Pearson相关分析.结果 病理观察可见干热组各时间点肺病理损伤较常温组病理损伤、蛋白渗出严重且肺组织病理学评分较高.两组肺组织匀浆NO质量摩尔浓度总体比较差异具有统计学意义(t=2.472,P＜0.05),干热组内各时间点比较差异具有统计学意义(F =6.77,P＜0.01),同一时间点干热组数值均大于常温组数值,干热组在2h达到最大值(3.35±0.23)μmol/g较常温组峰值出现早.两组iNOS mRNA表达量总体比较t检验差异具有统计学意义(t=3.619,P＜0.01),干热组组内各时间点比较差异具有统计学意义(F=12.34,P＜0.01),同一时间点干热组数值均大于常温组,干热组1.Sh时峰值出现,常温组则在2h时开始增加.两组肺组织匀浆NO质量摩尔浓度与iNOS mRNA表达量呈正相关(r=0.680、r=0.376),iNOS mRNA表达量与肺损伤病理学评分呈正相关(r=0.846、r=0.899).结论 在沙漠干热环境中创伤失血性休克继发性肺损伤时,肺脏损伤较常温环境下严重、较早,NO、iNOS在沙漠干热环境创伤失血性休克继发性肺损伤过程中起重要作用.     

大黄对大鼠肠缺血再灌注所致肺损伤过程肿瘤坏死因子、一氧化氮和磷脂酶A2的影响

目的：观察肿瘤坏死因子（ＴＮＦ）、内源性一氧化氮（ＮＯ）和磷脂酶Ａ２（ＰＬＡ２）在大鼠小肠缺血再灌注（ＩＲ）所致肺损伤发病过程中的作用,及大黄对ＴＮＦ、ＮＯ和ＰＬＡ２的影响,探讨大黄防治肠源性肺损伤的机制。方法：ＳＤ大鼠随机分为肠缺血再灌注组、假手术组、大黄治疗组和安慰剂组。以１２５Ｉ标记小牛血清白蛋白（ＢＳＡ）肺摄取指数作为评价肺损伤的指标,以髓过氧化物酶（ＭＰＯ）作为评价多形核白细胞（ＰＭＮ）在组织中聚集的指标,分别测定各组动物不同时间血浆、肺组织ＴＮＦ含量,血浆（血清）、肺及小肠组织内源性ＮＯ含量及ＰＬＡ２活性。结果：大黄可显著改善ＩＲ导致的低血压状态并明显抑制再灌注导致的肺ＭＰＯ活性升高（Ｐ＜０．０１）;抑制肠缺血和再灌注早期出现的血浆及肺组织ＴＮＦ水平升高（Ｐ＜０．０１）;抑制肠缺血期和再灌注期血清、肺及小肠组织ＰＬＡ２活性升高（Ｐ＜０．０５或Ｐ＜０．０１）及再灌注期的内源性ＮＯ释放（Ｐ＜０．０５或Ｐ＜０．０１）;降低肺毛细血管通透性（Ｐ＜０．０１）。结论：缺血再灌注早期应用大黄能明显防治大鼠ＩＲ所致的肺损伤,这种作用可能是通过抑制ＴＮＦ、内源性ＮＯ及ＰＬＡ２等介质的释放实现的。     

Hemodynamic and gas exchange responses to inhalation of nitric oxide in patients with the acute respiratory distress syndrome and in hypoxemic patients with chronic obstructive pulmonary disease

Objective: Inhalation of nitric oxide (NO) can improve oxygenation and decrease mean pulmonary artery pressure (MPAP) in patients with the acute respiratory distress syndrome (ARDS). It is not known whether inhaled NO exerts a similar effect in hypoxemic patients with chronic obstructive pulmonary disease (COPD). Design: Prospective clinical study. Setting: General intensive care unit in Sabadell, Spain. Patients: Nine mechanically ventilated COPD patients (mean age 72±2 years; forced expiratory volume in 1 s 0.91±0.11 l) and nine ARDS patients (mean age 57±6 years; mean lung injury score 2.8±0.1) Measurements and results: We measured hemodynamic and gas exchange parameters before NO inhalation (basal 1), during inhalation of 10 ppm NO (NO-10), and 20 min after NO was discontinued (in basal 2) in the ARDS group. In the COPD group, these parameters were measured before NO inhalation (basal 1), during different doses of inhaled NO (10, 20, and 30 ppm), and 20 min after NO was discontinued (basal 2). A positive response to NO was defined as a 20% increment in basal arterial partial pressure of oxygen (PaO₂). MPAP and pulmonary vascular resistance (PVR) decreased significantly, while other hemodynamic parameters remained unchanged after NO-10 in both groups. Basal oxygenation was higher in the COPD group (PaO₂/FIO₂ (fractional inspired oxygen) 190±18 mmHg) than in the ARDS group (PaO₂/FIO₂ 98±12 mmHg), (p<0.01). After NO-10, PaO₂/FIO₂ increased (to 141±17 mmHg, p<0.01) and Qva/Qt decreased (39±3 to 34±3%, p<0.01) in the ARDS group. There were no changes in PaO₂/FIO₂ and Qva/Qt when the NO concentration was increased to 30 ppm in the COPD group. In both groups, a correlation was found between basal MPAP and basal PVR, and between the NO-induced decrease in MPAP and in PVR. The NO-induced increase in PaO₂/FIO₂ was not correlated with basal PaO₂/FIO₂. In the ARDS group, six of the nine patients (66%) responded to NO and in the COPD group, two of nine (22%) (p=0.05). Conclusions: NO inhalation had similar effects on hemodynamics but not on gas exchange in ARDS and COPD patients, and this response probably depends on the underlying disease. Received: 19 December 1995 Accepted: 28 September 1996