scholarly journals Quantitative Measurement of Nasal Production of Nitric Oxide in Awake Humans

1995 ◽  
Vol 23 (6) ◽  
pp. 702-705 ◽  
Author(s):  
I. R. Jenkins ◽  
D. Langlois

The aim of this study was to determine, quantitiatively, the production of nitric oxide (NO) in the nose and nasopharynx. Subjects were instructed to perform a Valsalva manoeuvre with their mouth open as gas was aspirated from a closely fitting nasal CPAP mask by a chemiluminescence analyser (Sievers 270B, Sievers Instrument Corp. Boulder, Colorado, U.S.A.). Room air was free to flow in through the mouth and out through the nose and hence to the analyser. The manoeuvre was continued until a smooth plateau of at least 20 seconds in duration was achieved on a chart recorder. The mean plateau concentrations were 176 (±39.6) parts per billion (ppb) for males and 135.8 (±24.4) ppb for females. The mean male production of NO was 15.8 nanomol/min which was significantly different from that of females of 12.5 nanomol/min (Mann-Whitney U Test; P < 0.01). By measuring the concentration of NO in gas aspirated from the nose during Valsalva manoeuvre, we excluded the respiratory tract below the glottis from our sampling and as such results represent the portion of NO produced in the nose and nasopharynx. These findings suggest that nasally produced NO is produced in sufficient quantities to act as a continuous pulmonary vasodilator, being inspired preferentially into areas of greatest ventilation, thus perhaps acting to continually match ventilation to perfusion.

2016 ◽  
Vol 47 (5) ◽  
pp. 1348-1356 ◽  
Author(s):  
Sandrah P. Eckel ◽  
Zilu Zhang ◽  
Rima Habre ◽  
Edward B. Rappaport ◽  
William S. Linn ◽  
...  

Mechanisms for the adverse respiratory effects of traffic-related air pollution (TRAP) have yet to be established. We evaluated the acute effects of TRAP exposure on proximal and distal airway inflammation by relating indoor nitric oxide (NO), a marker of TRAP exposure in the indoor microenvironment, to airway and alveolar sources of exhaled nitric oxide (FeNO).FeNO was collected online at four flow rates in 1635 schoolchildren (aged 12–15 years) in southern California (USA) breathing NO-free air. Indoor NO was sampled hourly and linearly interpolated to the time of the FeNO test. Estimated parameters quantifying airway wall diffusivity (DawNO) and flux (J′awNO) and alveolar concentration (CANO) sources of FeNO were related to exposure using linear regression to adjust for potential confounders.We found that TRAP exposure indoors was associated with elevated alveolar NO. A 10 ppb higher indoor NO concentration at the time of the FeNO test was associated with 0.10 ppb higher average CANO (95% CI 0.04–0.16) (equivalent to a 7.1% increase from the mean), 4.0% higher J′awNO (95% CI −2.8–11.3) and 0.2% lower DawNO (95% CI −4.8–4.6).These findings are consistent with an airway response to TRAP exposure that was most marked in the distal airways.


2020 ◽  
Vol In Press (In Press) ◽  
Author(s):  
Nadia Elyassi ◽  
Ali Malekzadeh Shafaroudi ◽  
Pegah Nasiri ◽  
Mahmood Moosazadeh ◽  
Azam Nahvi

Context: Conflicting results have been reported in the literature concerning the relationship between salivary nitrous oxide concentration and dental caries in children. Metaanalysis studies aim to combine different studies and reduce the difference between the parameters by increasing the number of studies involved in the analysis process. Objectives: Accordingly, this meta-analysis study aimed at determining the relationship between salivary nitrous oxide concentration and dental caries in children. Methods: Databases were searched using the keywords “nitric oxide”, “salivary”, “Caries”, “DMFT Index”, “children”, “early childhood caries” and OR, AND and NOT operators. Quality assessment was then performed based on the Newcastle-Ottawa scale (NOS) checklist. The standardized mean difference (SMD) of DMFT, dmft, and salivary nitric oxide (NO) concentration was estimated. Results: Seven studies made a comparison between the mean salivary NO concentration in children with dental caries and that in the control group. In four studies, the mean salivary NO concentration in children with dental caries was lower, as compared to that in the control group. This difference was significant in all four studies. Also, the mean standardized difference of the salivary NO index was also estimated to be -0.11 (CI 95%: -1.77, 1.55). Conclusions: This meta-analysis study demonstrated that salivary NO concentration was not significantly related to dental caries. Moreover, since salivary NO concentration is affected by various factors, it is not sufficient to determine the likelihood of the incidence of caries.


2001 ◽  
Vol 85 (02) ◽  
pp. 245-249 ◽  
Author(s):  
John Horan ◽  
Charles Francis ◽  
Ann Falsey ◽  
John Kolassa ◽  
Brian Smith ◽  
...  

SummaryMortality rates attributable to cerebrovascular and ischemic heart disease increase among older adults during the winter. Prothrombotic changes in the hemostatic system related to seasonal factors, such as ambient temperature changes, and winter acute respiratory tract infections, may contribute to this excess seasonal mortality. A prospective nested case-control study was conducted to assess the impact of winter acute respiratory tract infections on fibrinogen, factor VII, factor VIIa, D-dimer, prothrombin fragment 1.2, PAI-1, soluble P-selectin and C-reactive protein (CRP) in older adults. The change in laboratory parameters from baseline (fall) to the time of infection in both middle-aged and elderly individuals was compared with matched non-infected controls. In older adult participants with winter acute respiratory tract infections, significant increases occurred in fibrinogen and C-reactive protein, but not in any other markers. The mean fibrinogen increased 1.52 g/L (38%) and the mean CRP increased 37 mg/L (370%) over baseline (both p < 0.001). In a multivariate analysis, both infection and season were associated with the increase in fibrinogen, but only infection was associated with the CRP increase. Old age magnified the increase in CRP but not in fibrinogen. Winter acute respiratory tract infections induce an exaggerated inflammatory response in older adults. The associated increase in fibrinogen, an independent risk factor for ischemic heart disease, may be partly responsible for the excess winter vascular mortality.


Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Cyndya A Shibao ◽  
Jorge E Celedonio ◽  
Latisha Gregory-Love ◽  
Claudia E Ramirez ◽  
Amy C Arnold ◽  
...  

CD36, a scavenger receptor expressed on endothelial cells, interacts with thrombospodin-1, a matrix protein that modulates nitric oxide-soluble guanylate cyclase (NO-sGC) signaling. CD36 genetic variants associate with endothelial dysfunction, atherosclerosis, hypertension and insulin resistance. A coding variant of CD36 (rs3211938, G/T genotype) that causes partial CD36 deficiency (50% reduction) is common (~18%) in African Americans (AA); however, it is unknown, if this genotype influences NO-dependent endothelial function. This study examined whether potentiating NO-sGC pathways with the phosphodiesterase 5 inhibitor, sildenafil citrate, improves endothelial function and insulin sensitivity in AA women with or without the G/T genotype. Forty-six AA women with metabolic syndrome (MetS) participated in a 4-week, parallel-arm, double-blind, and placebo-controlled study. Carefully matched subjects were randomly assigned to sildenafil citrate 20 mg TID versus placebo; sildenafil (n= 23, 42±10 years old, BMI 39±5 kg/m2, fasting insulin 15±8 uU/ml) and placebo (n=23, age 43±10, BMI 39±6 kg/m2, fasting insulin 14±10 uU/ml). Primary endpoints were insulin sensitivity and endothelial function measured by intravenous glucose tolerance test and flow mediated dilation, respectively. Treatment compliance was documented with plasma sildenafil levels (mean 57±50 ng/ml). There was no difference in insulin sensitivity (p=0.676) or flow-mediated dilation (p=0.649) between intervention groups. However, subgroup analyses showed a significant interaction between sildenafil citrate treatment and G/T genotype (p=0.018). Sildenafil citrate improved endothelial function in G/T carriers (the mean difference: 2.9, the 95% CI: -0.90 to 6.8, p = 0.126) and decreased endothelial function in T/T carriers (the mean difference: -2.6, the 95% CI: -5.1 to -0.1, p = 0.040). We conclude that the rs3211938 common CD36 genetic variant influences NO-dependent endothelial function in response to chronic treatment with phosphodiesterase 5 inhibition. Further studies are needed to determine if rs3211938 and other common CD36 genotypes influence endothelial function and the inter-individual variability in response to the drug.


Circulation ◽  
2018 ◽  
Vol 138 (Suppl_1) ◽  
Author(s):  
Yimin Hua ◽  
Yifei Li ◽  
Kaiyu Zhou

Objectives: We sought to analyze the outcomes of transcatheter patent ductus arteriosus (PDA) occlusion using a variety of devices in infants ≤ 6 mouths and discuss the transcatheter occlusion indication of PDA in early infants. Methods and Results: A total of 72 patients underwent successful transcatheter device closure. The mean age at catheterization was 4.9±1.8months (1-6 months) with a mean weight at catheterization of 5.1±1.9kg (1.9-6.7kg), the mean PDA diameter of 3.9±0.8mm (1.8-5.3mm),the mean systolic pulmonary arteriosus pressure of 55.7±8.9 mmHg (46-79mmHg). Among these suffered infants, companied with 72cases of growth retardation, 48 cases of recurrent lower respiratory tract infection, 35 cases associated with congestive heart failure, and 5 cases of respirator-oxygen-dependent. 4/6-8/10 PDA occluder was selected for transcatheter device closure, and intraoperative blood transfusion were performed in 46 cases. All subjects resulted with occluder position in good shape, no residual shunt; whileas 16 cases with aortic blood flow velocity increased slightly, 12 cases with left pulmonary artery blood flow velocity increased slightly just postoperation. And in follow-ups the increased velocity of and pulmonary blood flow gradually returned to normal. Follow-up data showed, all subjects resulted good outcomes with growth significantly improved, congestive heart failure cured and repeated lower respiratory tract infection significantly reduced postoperative. Conclusions: In experienced heart center, percutaneous closure of PDA should be considered even in infants ≤ 6 mouths. The indications include PDA infants with respirator-oxygen-dependent, congestive heart failure, and recurrent lower respiratory tract infection and growth retardation. Children underwent PDA occlusion would result with improved growth and development, recovered heart function and less lower respiratory tract infection.


2021 ◽  
pp. 261-292
Author(s):  
Daniel R. van Gijn ◽  
Jonathan Dunne

The larynx, trachea and bronchi develop embryologically from the foregut in the form of an outpouching during the fourth week of gestation. The larynx bridges the gap from the base of the tongue above, to the trachea below lying within the hypopharynx. It sits in the neck spanning the distance from the third to sixth cervical vertebrae. It is a complex respiratory organ composed of a cartilage framework, ligaments, intrinsic and extrinsic muscles and is lined by an epithelial mucous membrane continuous above with the pharynx and below with the trachea. Its primary function is protection of the lower respiratory tract against aspiration. It allows the generation of a high intrathoracic pressure required for coughing, straining and lifting (Valsalva manoeuvre) and phonation. The anatomy of the larynx can either be considered by its surgical division of the supraglottis, glottis and subglottis (these landmarks are important in the consideration of cancer spread).


2002 ◽  
Vol 282 (6) ◽  
pp. H2198-H2209 ◽  
Author(s):  
David B. Haitsma ◽  
Daphne Merkus ◽  
Jefrey Vermeulen ◽  
Pieter D. Verdouw ◽  
Dirk J. Duncker

Left ventricular (LV) dysfunction caused by myocardial infarction (MI) is accompanied by endothelial dysfunction, most notably a loss of nitric oxide (NO) availability. We tested the hypothesis that endothelial dysfunction contributes to impaired tissue perfusion during increased metabolic demands as produced by exercise, and we determined the contribution of NO to regulation of regional systemic, pulmonary, and coronary vasomotor tone in exercising swine with LV dysfunction produced by a 2- to 3-wk-old MI. LV dysfunction resulted in blunted systemic and coronary vasodilator responses to ATP, whereas the responses to nitroprusside were maintained. Exercise resulted in blunted systemic and pulmonary vasodilator responses in MI that resembled the vasodilator responses in normal (N) swine following blockade of NO synthase with N ω-nitro-l-arginine (l-NNA, 20 mg/kg iv). However, l-NNA resulted in similar decreases in systemic (43 ± 3% in N swine and 49 ± 4% in MI swine), pulmonary (45 ± 5% in N swine and 49 ± 4% in MI swine), and coronary (28 ± 4% in N and 35 ± 3% in MI) vascular conductances in N and MI swine under resting conditions; similar effects were observed during treadmill exercise. Selective inhibition of inducible NO synthase with aminoguanidine (20 mg/kg iv) had no effect on vascular tone in MI. These findings indicate that while agonist-induced vasodilation is already blunted early after myocardial infarction, the contribution of endothelial NO synthase-derived NO to regulation of vascular tone under basal conditions and during exercise is maintained.


1997 ◽  
Vol 272 (1) ◽  
pp. L44-L50 ◽  
Author(s):  
X. J. Yuan ◽  
R. T. Bright ◽  
A. M. Aldinger ◽  
L. J. Rubin

Nitric oxide (NO) is a potent endothelium-derived pulmonary vasodilator. Serotonin (5-HT; 10-50 microM) constricts pulmonary artery (PA) by releasing Ca2+ from intracellular stores and promoting Ca2+ influx through Ca2+ channels in PA smooth muscle cells (PASMC). The effect of NO on 5-HT-induced increase in cytosolic free Ca2+ concentration ([Ca2+]i) in rat PASMC was investigated to elucidate whether inhibition of agonist-mediated Ca2+ rise is involved in the NO-mediated pulmonary vasodilation. The 5-HT-induced increase in [Ca2+]i was characterized by a transient (because of Ca2+ release from intracellular stores) followed by a plateau (because of Ca2+ influx). Removal of extracellular Ca2+ eliminated the 5-HT-induced [Ca2+]i plateau, but insignificantly affected the [Ca2+]i transient. In some of the PASMC bathed in the Ca(2+)-containing or Ca(2+)-free solution, 5-HT also induced Ca2+ oscillations. Pretreatment of the cells with 10 microM cyclopiazonic acid (CPA) abolished, whereas 10 mM caffeine negligibly affected, the 5-HT-induced [Ca2+]i transients in the absence of external Ca2+. Authentic NO (approximately 0.3 microM) reversibly diminished 5-HT-induced [Ca2+]i transients but augmented CPA-induced Ca2+ release in the absence of extracellular Ca2+. NO also significantly inhibited 5-HT-induced [Ca2+]i plateau in PASMC bathed in Ca(2+)-containing solution, suggesting that NO inhibits both agonist-induced Ca2+ release from the CPA-sensitive Ca2+ stores and Ca2+ influx from extracellular fluid. These data suggest that NO-induced inhibition of the evoked increases in [Ca2+]i and augmentation of Ca2+ sequestration into intracellular stores in PASMC are involved in the mechanisms by which NO causes pulmonary vasodilation.


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