Identification of vasopressor constituents of amniotic fluid in pregnancy toxaemia

Summary The vasopressor activity of human amniotic fluid was assessed in 46 primigravidas during the third trimester of pregnancy. The subjects included 20 normal and 26 cases of pregnancy toxaemia. For identification of the vasoptessor activity of the amniotic fluid, blood pressure measurements were made in the intact rat, and the smooth muscle contraction of the rat ascending colon preparation was determinedin vitro. The samples of amniotic fluid showing vasoptessor activity were lyophilized and subjected to gel filtration using Sephadex G-100. The various fractions thus obtained were monitored at 280 nm and the pressor activity was re-estimated. It was observed that most of the pressor activity of the amniotic fluid of the toxaemic patients was capable of causing contraction of the rat colon as well as a significant rise in the systolic blood pressure of the intact rat. Furthermore, this activity was found to be heat-labile and was completely blocked by cinnarizine. Fractionation of the amniotic fluid showing vasopressor activity by gel filtration further substantiated the findings reported above. On the basis of these results it was concluded that the pressor activity of the amniotic fluid was due to the presence of an angiotensin II-like substance. Its concentration was found to be higher in the toxaemic group than in normotensive subjects.     

颅脑损伤后急性期脑脊液中一氧化氮及其合成酶的动态观察

目的：检测一氧化氮（NO）及其合成酶（NOS）在颅脑损伤后急性期脑脊液中的变化,探讨了其临床意义,方法：采用检测NO的中间代谢产物亚硝酸盐来反映NO及放射强度测定法测定NOS活性,分别测定颅脑损伤后急性期脑脊液中NO和NOS变化,并行健康对照,结果：颅脑损伤后NO及NOS脑脊液中浓度第1天即增高,NO第3天达到高峰后开始下降,至第10天仍高于正常对照,NOS于损伤后第1天开始升高,至第10天仍高于正常对照组,结论：NO和NOS参与了颅脑损伤的病理生理过程,动态观察提示NO可能和颅脑损伤病情程度有关。     

Plasma nitrite concentration decreases after hyperoxia-induced oxidative stress in healthy humans

The aim of this study was to measure plasma nitrite, the biochemical marker of endothelial nitric oxide (^?NO) synthesis, before and after hyperoxia, in order to test the hypothesis that hyperoxia‐induced vasoconstriction is a consequence of reduced bioavailability of ^?NO caused by elevated oxidative stress. Ten healthy men breathed 100% normobaric O₂ for 30 min between 15th and 45th min of the 1‐h study protocol. Plasma nitrite and malondialdehyde (MDA), arterial stiffness (indicated by augmentation index, AIx) and arterial oxygen (P_tcO₂) pressure were measured at 1st, 15th, 45th and 60th minute of the study. Breathing of normobaric 100% oxygen during 30 min caused an increase in P_tcO₂ (from 75 ± 2 to 412 ± 25 mm Hg), AIx (from ?63 ± 4 to ?51 ± 3%) and MDA (from 152 ± 13 to 218 ± 15 nm ) values and a decrease in plasma nitrite (from 918 ± 58 to 773 ± 55 nm ). During the 15‐min recovery phase, plasma nitrite, AIx and MDA values remained altered. This study suggests that the underlying mechanism of hyperoxia‐induced vasoconstriction may involve reduced ^?NO bioavailability caused by elevated and sustained oxidative stress.     

脑脊液置换对蛛网膜下腔出血患者血清一氧化氮及内皮素的影响

目的：了解脑脊液置换对蛛网膜下腔出血（ＳＡＨ）患者外周血一氧化氮（ＮＯ）和内皮素（ＥＴ）的影响。方法：对１７例ＳＡＨ患者进行脑脊液置换，并对治疗前后的ＮＯ和ＥＴ水平进行观察。结果：脑脊液置换后第４日和第７日外周血ＮＯ水平分别由（４．４５±１．０２）μｍｏｌ／Ｌ升高至（８．０１±１．０１）μｍｏｌ／Ｌ和（７．９３±１．８７）μｍｏｌ／Ｌ，差异有极显著性（Ｐ均＜０．０１）；ＥＴ水平由（１２．３２±２．２７）ｎｇ／Ｌ下降至（５．５６±０．７５）ｎｇ／Ｌ和（６．０２±１．１０）ｎｇ／Ｌ，差异有极显著性（Ｐ均＜０．０１）。结论：脑脊液置换是治疗ＳＡＨ的有效方法。     

The influence of pregnancy on endothelium-derived nitric oxide mediated relaxations in isolated human resistance vessels

Summary— Pregnancy is associated with drastic hemodynamic adaptations, including a decrease in peripheral resistance. Vascular resistance is substantially influenced by endothelium-derived nitric oxide (NO). This study was designed to investigate whether pregnancy might influence endothelium-derived NO-mediated relaxations in human resistance arteries. Reactivity of isolated human subcutaneous arteries, dissected out of abdominal fat from women who underwent a laparotomy or cesarean section, was studied using a small vessel myograph. Addition of acetylcholine (1 nM–10 μM) or bradykinin (1 nM–10 μM) to precontracted preparations elicited concentration-dependent relaxation responses that were dependent on the presence of the endothelium and were partially inhibited by the NO-synthase inhibitor nitro-L-arginine (0.1 mM). The relaxations to acetylcholine and bradykinin were similar in vessels isolated from pregnant and non-pregnant women. Nitro-L-arginine (0.1 mM) had no influence on basal tone and had a similar inhibitory influence on the endothelium-mediated relaxations in vessels from non-pregnant and pregnant women. These results indicate that the influence of endothelium-derived NO in human subcutaneous resistance arteries is not altered at the end of pregnancy.     

Exhaled nitric oxide and its long‐term variation in healthy non‐smoking subjects

Exhaled nitric oxide (NOexp) is an indicator of inflammation in the airways. Reference values obtained from healthy adults or information on long‐term variation of NOexp are not yet available. The aims of this pilot study were to collect values of NOexp from a selected group of healthy adults and to assess their long‐term variation. We studied 26 healthy subjects (age 21–48, 16 male, 10 female) with normal findings in flow‐volume spirometry, pulmonary diffusing capacity, relative amount of blood eosinophils, chest X‐ray and ECG at rest. NOexp was determined according to the European Respiratory Society guidelines during slow expiration against an airflow resistance. The measurements were repeated after 7 (n=13) and 23 days (n=17). The mean value of NOexp (n=26) was 6·9 ng g^–1 (95% confidence interval, 6·0–7·9 ng g^–1). The upper limit of intra‐individual variation (+2 SD) was 11·9 ng g^–1 and the lower limit (–2 SD) 1·9 ng g^–1, respectively. The mean (SD) value of NO production (NO output) was 39·1 pmol s^–1 (20 pmol s^–1). We found no correlation between NOexp and age (r=–0·06, P=0·78) and no association of NOexp with the gender (male vs. female, P=0·40). The intraindividual coefficient of variation (CoV) was 15·8% of NOexp and 20·7% of NO output within the interval of 7 days. CoV was 16·8% of NOexp and 18% of NO output within the interval 23 days. The results suggest that NOexp values over 12 ng g^–1 are abnormally high in healthy subjects. According to the results the change of NOexp by 30–35% or more within the interval of 1–3 weeks would be abnormal.     

大鼠创伤性脑水肿一氧化氮及其合成酶的变化

目的：探讨脑损伤后一氧化氮（ＮＯ）及一氧化氮合酶（ＮＯＳ）与脑水肿的关系。方法：建立大鼠创伤性脑水肿模型,按不同时间点处死动物,测定其脑含水量及静脉血ＮＯ 和脑组织中ＮＯＳ。结果：脑创伤后脑含水量随静脉血ＮＯ的增加而增加,组织ＮＯＳ则随ＮＯ 的增加而下降。结论：创伤性脑水肿与血ＮＯ 有密切相关性,组织中ＮＯＳ则是该过程的可能催化剂     

亚硝基谷胱甘肽对冰冻血小板聚集及一氧化氮含量的影响

本研究探讨亚硝基谷胱甘肽(GSNO)对冷冻血小板聚集及一氧化氮(NO)含量的影响。用血小板聚集仪对血小板的聚集率进行测定,用硝酸还原酶法对NO含量进行检测。结果表明,新鲜液态血小板的聚集率为(63.44±2.96)%,冷冻血小板的聚集率为(35.47±2.93)%,加入GSNO后的冷冻血小板聚集率为(24.43±3.07)%。32例正常献血者新鲜液态血小板的NO浓度为(31.59±16.88)μmol/L。32例冷冻血小板的NO浓度为(22.16±6.38)μmol/L,明显低于新鲜液态血小板组。32例加入GSNO的冷冻血小板NO浓度为(45.64±6.31)μmol/L,明显高于新鲜液态血小板组。结论:GSNO增加了冷冻血小板NO的浓度,抑制血小板的聚集,保持血小板的功能,可以用作冷冻保护剂。     

生脉饮对内毒素诱导急性肺损伤大鼠一氧化氮及其合酶的影响

目的:探讨一氧化氮(NO)和诱生型一氧化氮合酶(iNO S)在脂多糖(LPS)诱导大鼠急性肺损伤(AL I)中的作用及生脉饮对其的影响。方法:雄性W istar大鼠按随机数字表法分为对照组、AL I组、生脉饮组、地塞米松组。舌下静脉注射LPS复制AL I模型。观察大体标本、组织病理以及肺湿/干重比、支气管肺泡灌洗液中中性粒细胞比、蛋白含量、肺毛细血管通透性和肺泡通透性指数等生物学指标。测定血浆NO和肺组织匀浆iNO S活性。结果:与对照组比较,AL I组肺组织病理显示肺间质及肺泡有明显的损伤和细胞浸润,各生物学指标及NO和iNO S显著升高(P<0.05或P<0.01);与AL I组比较,地塞米松组和生脉饮组肺组织病理明显减轻,各生物学指标及NO、iNO S也相应下降(P<0.05或P<0.01)。结论:地塞米松和生脉饮两种药物对LPS诱导的AL I具有保护作用,其机制可能是通过抑制NO水平和iNO S活性实现。     

Low‐intensity ultrasound increases endothelial cell nitric oxide synthase activity and nitric oxide synthesis

Summary. Low‐intensity ultrasound (US) increases tissue perfusion in ischemic muscle through a nitric oxide (NO)‐dependent mechanism. We have developed a model to expose endothelial cells to well‐characterized acoustic fields in vitro and investigate the physical and biological mechanisms involved. Human umbilical vein endothelial cells (HUVEC) or bovine aortic endothelial cells (BAEC) were grown in tissue culture plates suspended in a temperature‐controlled water bath and exposed to US. Exposure to 27 kHz continuous wave US at 0.25 W cm^?2 for 10 min increased HUVEC media NO by 102 ± 19% (P < 0.05) and BAEC by 117 ± 23% (P < 0.01). Endothelial cell NO synthase activity increased by 27 ± 24% in HUVEC and by 32 ± 16% in BAEC (P < 0.05 for each). The cell response was rapid with a significant increase in NO synthesis by 10 s and a maximum increase after exposure for 1 min. By 30 min post‐exposure NO synthesis declined to baseline, indicating that the response was transient. Unexpectedly, pulsing at a 10% duty cycle resulted in a 46% increase in NO synthesis over the response seen with continuous wave US, resulting in an increase of 147 ± 18%. Cells responded to very low intensity US, with a significant increase at 0.075 W cm^?2 (P < 0.01) and a maximum response at 0.125 W cm^?2. US caused minor reversible changes in cell morphology but did not alter proliferative capacity, indicating absence of injury. We conclude that exposure of endothelial cells to low‐intensity, low‐frequency US increases NO synthase activity and NO production, which could be used to induce vasodilatation experimentally or therapeutically.     

Different plasma levels of nitric oxide in arterial and venous blood

Experimental investigations suggest that a basal release of nitric oxide (NO) occurs in arterial but not in venous endothelium. We therefore decided to compare plasma levels of NO in the arterial and venous circulation. Parallel blood samples were drawn from the radial artery and brachial vein in 15 healthy drug-free women. Nitric oxide levels were assessed by measuring plasma levels of nitrite and nitrate, the two stable oxidation products of NO metabolism. Plasma levels of NO metabolites in arterial blood were significantly higher than in the paired venous blood samples (45·1 ± 17·7 versus 22·5 ± 8·5 μmol l^?1, respectively, mean ± SD). The results of this preliminary study strongly suggest that the endothelial release of NO is probably different in arteries and veins in vivo; this is also consistent with previous literature indicating that basal release of NO occurs mainly from the endothelium of arteries but not from that of veins.     

超声对羊水内带状回声的诊断价值

目的探讨超声诊断羊水内带状回声的临床价值。方法 54例伴有羊水内带状回声的中晚期妊娠的孕妇,超声观察带状回声的超声特点及胎儿、附属物情况,询问病史并追踪随访。结果 54例羊水内带状回声中,双胎间隔膜18例,羊膜片16例,不全纵隔子宫9例,羊膜、绒毛膜未融合7例,轮状胎盘2例,羊膜带综合征2例。结论羊水内带状回声的形成有多种原因,有的为正常生理现象或良性过程,有的为严重病理现象,直接影响胎儿预后,做出正确诊断对指导临床有重要的价值。     

Exhaled nitric oxide during incremental and constant workload exercise in chronic cardiac failure

BACKGROUND: Nitric oxide (NO) is present in exhaled breath and produced by the pulmonary vascular endothelium as a potent vasodilator. Exercise is normally associated with pulmonary vasodilatation and a decrease in pulmonary vascular resistance to accommodate the increase in cardiac output. If production of NO is impaired in patients with chronic congestive cardiac failure (CCF), this might contribute to their exercise intolerance. PATIENTS AND METHODS: We quantified NO production (V NO) in 12 patients with chronic stable CCF and 12 controls, at rest and during incremental cardiopulmonary exercise on a treadmill, and at a later date during constant workload exercise. RESULTS: Patients had reduced V NO compared with controls during incremental exercise [381 (180) vs. 777 (275) nL min-1; mean (SD); P < 0.0001] but at constant workload V NO was similar between the two groups [353 (124) vs. 389 (189) nL min-1; P = 0.25]. Plasma levels of nitrate, the stable end-product of NO production, were significantly higher in patients [resting value 46.1 (21.6) vs. 23.0 (10.0) microM; P = 0.004] and were not influenced by exercise. CONCLUSION: Impaired NO-mediated pulmonary vasodilatation does not appear to contribute to exercise limitation in CCF. Alternatively, the lower NO production observed during maximal exercise in the patient group compared with controls may reflect a reduced incremental response of a system that is already abnormally activated in heart failure.     

呼出气一氧化氮联合相关因素对咳嗽变异性哮喘的诊断价值评价

目的 :评价呼出气一氧化氮(Fe NO)检测单独或联合咳嗽变异性哮喘(cough variant asthma,CVA)相关因素对诊断CVA的有效性和准确性。方法:连续纳入2010年8月至2011年10月本院呼吸科门诊因慢性咳嗽行支气管激发试验检查的患者297例,记录病史并测定呼出气Fe NO水平,以支气管激发试验阳性作为CVA诊断的金标准,绘制ROC曲线,探讨诊断CVA的Fe NO临界点。建立Logisitic回归模型,通过分析筛选与CVA相关的因素,根据ROC曲线评价Fe NO联合其他相关因素对CVA的诊断价值。结果:145例患者支气管激发试验阳性并排除其他疾病被诊断为CVA(哮喘组),152例支气管激发试验阴性患者诊断为非哮喘的慢性咳嗽(非哮喘组)。1哮喘组患者Fe NO水平明显高于非哮喘组[(45.33±38.86)ppb比(26.28±23.86)ppb,P     

Oral nitric oxide during plaque deposition

BACKGROUND: Nitric oxide (NO) is one of the most powerful antibacterial compounds. We investigated if NO oral production increases during dental plaque deposition. MATERIALS AND METHODS: Oral NO and salivary nitrite were measured in 31 healthy subjects - 11 smokers and 20 nonsmokers - with natural healthy teeth, in the morning after tooth cleaning (baseline), after withdrawal of oral hygiene for 24 h and again after tooth cleaning. RESULTS: NO and nitrite were significantly higher during plaque deposition than with clean teeth: mean NO values +/- SEM were 44.3 +/- 4.9 parts per billion (ppb) at baseline, 58.8 +/- 3.7 ppb with plaque and 43.6 +/- 3.7 ppb after tooth cleaning, P < 0.05; nitrite values were 32.9 +/- 5.5 microm at baseline, 66.4 +/- 8.2 with plaque and 37.5 +/- 5.5 after tooth cleaning, P < 0.01. During plaque deposition, oral NO was significantly directly related to salivary nitrite (r = 0.497, P = 0.002) and so were their respective changes after tooth cleaning (r = 0.577, P < 0.001). Smokers had significantly lower oral NO than nonsmokers, with both clean and dirty teeth (P < 0.001), and higher bacteria counts in the plaque (38.6 +/- 11.5 vs. 19.9 +/- 2.3, P = 0.046). CONCLUSIONS: Oral NO production increases during de novo deposition of dental plaque. NO might be an early host defence mechanism against bacterial proliferation in the plaque. Such a mechanism is inhibited by cigarette smoking.     

Nasal nitric oxide concentration is decreased in heart failure patients receiving nitrates

Summary— Nitric oxide (NO) is a free radical gas and a short-lived messenger which has many paracrine functions. Direct assessment of NO production is very difficult in vivo. However, the paranasal cavities generate a high amount of NO which diffuses in the nasal cavity where it can be easily measured. Several studies have suggested alterations of the NO production in heart failure. Thus, we assessed nasal NO concentration in normal subjects and in heart failure patients. The nasal NO concentration averaged 227 ± 10 ppb in the control group (n = 20), and 210 ± 10, 198 ± 20 and 159 ± 54 ppb in New York Heart Association (NYHA) class II (n = 30), III (n = 28) and IV (n = 7) patients, respectively (mean ± standard error [SE], not significant using analysis of variance [ANOVA]). Nasal NO level was not influenced by age, sex or etiology of the heart failure or by treatment with frusemide, angiotensin-converting enzyme inhibitor or digoxin. However, treatment with NO-releasing drugs (nitrates or molsidomine) significantly decreased the nasal NO level in heart failure patients. A two-way ANOVA revealed that treatment with a NO-releasing drug influenced nasal NO concentration (P = 0.0005), whereas NYHA class did not (P = 0.23), with a trend towards an interaction between the two parameters (P = 0.09): the inhibitory effect of NO-releasing drug on nasal NO concentration was more pronounced in severe heart failure. In an additional group of 12 patients (NYHA class II or III), the nasal NO concentration was 174 ± 19 ppb during NO-releasing drug treatment and increased to 231 ± 27 ppb 3 days after withdrawal of the nitrates (P = 0.0007 using paired t-test). Conversely, the nasal NO concentration in another group of seven patients (NYHA class II or III) was 219 ± 32 ppb without nitrate treatment and decreased to 188 ± 28 ppb 7 days after nitrate addition (P = 0.02 using paired (test). In contrast, the nasal NO concentration in another group of ten ischemic patients without heart failure was 203 ± 25 ppb without nitrate treatment and was similar (207 ± 28 ppb) 7 days after nitrate addition (not significant using paired t-test). In conclusion, nasal NO production is normal in heart failure, except in patients receiving NO-releasing drugs. Nasal NO concentration could be useful for investigating the mechanism(s) by which exogenous NO donors decrease endogenous NO production.     

Renin substrate in human amniotic fluid

Purified human amniotic fluid renin substrate (RS) was compared to purified plasma RS. RS in plasma and amniotic fluid were similar in molecular weight, isoelectric point and immunological properties.

Immunoreactivity of radio-iodinated amniotic fluid RS was lower than that of plasma RS. Measured by direct radioimmunoassay, RS-levels were only 10–22% of those obtained with indirect assay in 22 amniotic fluid samples. This difference suggests that amniotic fluid RS is less immunoreactive than plasma RS, possibly due to biochemical alteration or complex formation. No such difference in immunoreactivity was noticed in RS of decidual and placental cytosolic fraction.