Nitric oxide production and absorption in trachea, bronchi, bronchioles, and respiratory bronchioles of humans

1999 ◽  
Vol 86 (1) ◽  
pp. 159-167 ◽  
Author(s):  
Arthur B. DuBois ◽  
Patrick M. Kelley ◽  
James S. Douglas ◽  
Vahid Mohsenin
Keyword(s):  
Nitric Oxide ◽  
Breath Holding ◽  
No Production ◽  
Production Rates ◽  
Oral Production ◽  
Clean Air ◽  
Equilibrium Concentrations ◽  
The Mean ◽  
Young Subjects ◽  
No Absorption

Different volumes of dead-space gas were collected and analyzed for nitric oxide (NO) content, either immediately after inspiration or after a period of breath holding on clean air or NO mixtures. This allowed calculation of NO equilibrium, NO production, and NO absorption. In seven young, healthy, adult nonsmokers, the mean NO equilibrium values in parts per billion (ppb) were 56 ± 11 (SE) in the trachea, 37 ± 6 in the bronchi, 21 ± 3 in the bronchioles, and 16 ± 2 in the respiratory bronchioles. At any given NO concentration, the NO absorption rate (in nl/min) equaled the NO concentration (in ppb) times A (the absorption coefficient in l/min). A values (in l/min) were 0.11 ± 0.01 in the trachea, 0.17 ± 0.04 in the bronchi, 0.66 ± 0.09 in the bronchioles, and 1.35 ± 0.32 in the respiratory bronchioles. NO equilibrium concentrations and production rates in one 74-yr-old subject were three to five times as high as those found in the young subjects. Mouth equilibrium NO concentrations were 3 and 6 parts per million in two subjects who had oral production rates of 6 and 23 nl/min, respectively. In conclusion, production and absorption of NO occur throughout the first 450 ml of the airways.

scholarly journals Simultaneous measurement of nitric oxide production by conducting and alveolar airways of humans

1999 ◽  
Vol 87 (4) ◽  
pp. 1532-1542 ◽  
Author(s):  
Anthony P. Pietropaoli ◽  
Irene B. Perillo ◽  
Alfonso Torres ◽  
Peter T. Perkins ◽  
Lauren M. Frasier ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Normal Subjects ◽  
Breath Holding ◽  
No Production ◽  
Large Contribution ◽  
Flow Rates ◽  
Expiratory Flow ◽  
Human Airways ◽  
Conducting Airways ◽  
Expiratory Flow Rates

Human airways produce nitric oxide (NO), and exhaled NO increases as expiratory flow rates fall. We show that mixing during exhalation between the NO produced by the lower, alveolar airways (V˙l NO) and the upper conducting airways (V˙u NO) explains this phenomenon and permits measurement ofV˙l NO,V˙u NO, and the NO diffusing capacity of the conducting airways (Du NO). After breath holding for 10–15 s the partial pressure of alveolar NO (Pa) becomes constant, and during a subsequent exhalation at a constant expiratory flow rate the alveoli will deliver a stable amount of NO to the conducting airways. The conducting airways secrete NO into the lumen (V˙u NO), which mixes with Pa during exhalation, resulting in the observed expiratory concentration of NO (Pe). At fast exhalations, Pa makes a large contribution to Pe, and, at slow exhalations, NO from the conducting airways predominates. Simple equations describing this mixing, combined with measurements of Pe at several different expiratory flow rates, permit calculation of Pa,V˙u NO, and Du NO.V˙l NOis the product of Pa and the alveolar airway diffusion capacity for NO. In seven normal subjects, Pa = 1.6 ± 0.7 × 10−6 (SD) Torr,V˙l NO= 0.19 ± 0.07 μl/min,V˙u NO= 0.08 ± 0.05 μl/min, and Du NO = 0.4 ± 0.4 ml ⋅ min−1 ⋅ Torr−1. These quantitative measurements ofV˙l NOandV˙u NOare suitable for exploring alterations in NO production at these sites by diseases and physiological stresses.

scholarly journals Determination of dissolved nitric oxide in coastal waters of the Yellow Sea off Qingdao

2017 ◽  
Author(s):  
Chun-Ying Liu ◽  
Wei-Hua Feng ◽  
Ye Tian ◽  
Gui-Peng Yang ◽  
Pei-Feng Li ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Detection Limit ◽  
Coastal Waters ◽  
Yellow Sea ◽  
The Yellow Sea ◽  
No Production ◽  
Spatial Distributions ◽  
Production Rates ◽  
Temporal And Spatial

Abstract. We developed a new method for the determination of dissolved nitric oxide (NO) in discrete seawater samples based on a combination of a purge-and-trap set-up and fluorometric detection of NO. 2,3-diaminonaphthalene (DAN) reacts with NO in seawater to form the highly fluorescent 2,3-naphthotriazole (NAT). The fluorescence intensity was linear for NO concentrations in the range from 0.14 nmol L−1 to 19 nmol L−1. We determined a detection limit of 0.068 nmol L−1, an average recovery coefficient of 83.8 % (80.2–90.0 %), and a relative standard deviation of ±7.2 %. With our method we determined for the first time the temporal and spatial distributions of NO surface concentrations in coastal waters of the Yellow Sea off Qingdao and in Jiaozhou Bay during a cruise in November 2009. The concentrations of NO varied from below the detection limit to 0.50 nmol L−1 with an average of 0.26 ± 0.14 nmol L−1. NO surface concentrations were generally enhanced significantly during daytime implying that NO formation processes such as NO2− photolysis are much higher during daytime than chemical NO consumption which, in turn, lead to a significant decrease of NO concentrations during nighttime. In general, NO surface concentrations and measured NO production rates were higher compared to previously reported measurements. This might be caused by the high NO2− surface concentrations encountered during the cruise. Moreover, additional measurements of NO production rates implied that the occurrence of particles and a temperature increase can enhance NO production rates. With the method introduced here we have a reliable and comparably easy to use method at hand to measure oceanic NO surface concentrations which can be used to decipher both its temporal and spatial distributions as well as its biogeochemical pathways in the oceans.

Nitric oxide contributes to desipramine- induced hypotension in rats

1996 ◽  
Vol 15 (4) ◽  
pp. 320-328 ◽  
Author(s):  
PR Pentel ◽  
W. Wananukul ◽  
W. Scarlett ◽  
DE Keylerl
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Survival Time ◽  
Control Treatment ◽  
No Production ◽  
No Donor ◽  
Induced Hypotension ◽  
Mean Survival Time ◽  
Anesthetized Rats ◽  
The Mean

1 Anesthetized rats received the TCA desipramine (DMI) 60 mg kg-1 i.p. Administration of the nitric oxide synthase (NOS) inhibitor NG-nitro-L-arginine methyl ester-(L-NAME) 15 min after DMI reversed hypotension within 5 min (P < 0.05). In contrast to its beneficial effect on blood pressure, L-NAME worsened DMI-induced prolongation of the electrocardiographic QRS interval. Dexamethasone, an inhibitor of NOS induction, did not prevent DMI-induced hypotension. 2 To study the effect of L-NAME on survival, DMI was administered to anesthetized rats as a continuous i.v. infusion until death. Despite initially improving blood pressure, L-NAME decreased the mean survival time by 33% (P < 0.01) compared to control treatment. Adminis tration of the nitric oxide (NO) donor nitroglycerine to rats during DMI infusion likewise decreased the mean survival time. 3 L-NAME partially reversed the hypotensive effect of nitroprusside in both anesthetized and awake rats. 4 These data suggest that NO production attributable to constitutive NOS ( cNOS) activity aggravates the hypoten sion associated with DMI toxicity in the anesthetized rat, and contributes to the pathophysiology of this overdose. The shortened survival time produced by both increasing and decreasing NO production suggests that cNOS activity during DMI overdose is regulated and adaptive. Ongoing cNOS activity also contributed to nitroprusside-induced hypotension, and may represent a feature common to other drug-induced hypotensive states.

scholarly journals Impact of Energetic Electron Precipitation on the Upper Atmosphere: Nitric Monoxide

2017 ◽  
Vol 11 (1) ◽  
pp. 88-104 ◽  
Author(s):  
A. Vialatte ◽  
M. Barthélemy ◽  
J. Lilensten
Keyword(s):  
Nitric Oxide ◽  
Solar Activity ◽  
Energetic Electron ◽  
Auroral Zone ◽  
Upper Atmosphere ◽  
Electron Precipitation ◽  
No Production ◽  
Neutral Atmosphere ◽  
Heating Rates ◽  
Production Rates

Background:Nitric oxide concentration in the upper atmosphere is known to be highly dependent on the solar activity. It can be transported to the stratosphere by the atmospheric circulation. In the stratosphere it is responsible for the destruction of ozone and consequently stratospheric heating rates are affected. This is one of the mechanisms by which solar variability has been suspected to drive variability in the energetic budget of the Earth climate. Therefore, it is essential to know every physical and chemical processes leading to the production or to a destruction of nitric oxide.Aim:The aim of this work is to calculate the production rate of NO+and some of the NO electronic states created by electron impact on NO at night in the auroral zone using an electron transport code.Conclusion:We study this variability under different precipitation conditions and taking into account the variability of the neutral atmosphere with the geomagnetic and solar activity. We find that the energetic electron precipitation has a very small effect on the absolute value of the NO+and NO* production rates. In order to help further research to consider the effect of NO+and NO*, we provide a table of all the production rates in a medium solar and geomagnetic activity case.

Determination of production of nitric oxide by lower airways of humans—theory

1997 ◽  
Vol 82 (4) ◽  
pp. 1290-1296 ◽  
Author(s):  
Richard W. Hyde ◽  
Edgar J. Geigel ◽  
Albert J. Olszowka ◽  
John A. Krasney ◽  
Robert E. Forster ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Barometric Pressure ◽  
Open Circuit ◽  
Capillary Blood ◽  
Breath Holding ◽  
No Production ◽  
Pulmonary Capillary ◽  
Determining Factors ◽  
Pulmonary Capillary Blood ◽  
Lower Airways

Hyde, Richard W., Edgar J. Geigel, Albert J. Olszowka, John A. Krasney, Robert E. Forster II, Mark J. Utell, and Mark W. Frampton.Determination of production of nitric oxide by the lower airways of humans—theory. J. Appl. Physiol.82(4): 1290–1296, 1997.—Exercise and inflammatory lung disorders such as asthma and acute lung injury increase exhaled nitric oxide (NO). This finding is interpreted as a rise in production of NO by the lungs (V˙no) but fails to take into account the diffusing capacity for NO (Dno) that carries NO into the pulmonary capillary blood. We have derived equations to measureV˙no from the following rates, which determine NO tension in the lungs (Pl) at any moment from 1) production (V˙no); 2) diffusion, where Dno(Pl) = rate of removal by lung capillary blood; and 3) ventilation, whereV˙a(Pl)/(Pb− 47) = the rate of NO removal by alveolar ventilation (V˙a) and Pb is barometric pressure. During open-circuit breathing when Pl is not in equilibrium, d/d tPl[V l / (Pb − 47)] (where V l is volume of NO in the lower airways) =V˙no− Dno(Pl) −V˙a(Pl)/(Pb− 47). When Pl reaches a steady state so that d/d t = 0 andV˙a is eliminated by rebreathing or breath holding, then Pl =V˙no/Dno. Pl can be interpreted as NO production per unit of Dno. This equation predicts that diseases that diminish Dno but do not alterV˙no will increase expired NO levels. These equations permit precise measurements of V˙no that can be applied to determining factors controlling NO production by the lungs.

scholarly journals Nitric Oxide Production is More Prominent in off-Pump than in On-Pump Coronary Artery Bypass Surgery

2007 ◽  
Vol 35 (4) ◽  
pp. 505-509 ◽  
Author(s):  
C. Mitaka ◽  
K. Yokoyama ◽  
T. Imai
Keyword(s):  
Nitric Oxide ◽  
Cardiopulmonary Bypass ◽  
Coronary Artery ◽  
Coronary Artery Bypass ◽  
Artery Bypass ◽  
No Production ◽  
Excretion Ratio ◽  
Off Pump ◽  
Significant Difference ◽  
The Mean

The aim of our study was to elucidate the extent to which cardiopulmonary bypass contributes to endogenous nitric oxide (NO) production in patients undergoing coronary artery bypass grafts (CABG). One-hundred-and-sixteen patients undergoing elective CABG with (on-pump, n=66) and without cardiopulmonary bypass (off-pump, n=50) were included. Urinary nitrite/nitrate (NOx) excretion was measured as an index of endogenous NO production during the first two postoperative days. Haemodynamic profiles, serum CK-MB and C-reactive protein (CRP) concentrations were measured after the operation. There was no significant difference in urinary NOx/creatinine (Cr) excretion on day one post CABG. The mean urinary NOx/Cr excretion ratio significantly (P <0.01) decreased from days one to two in the on-pump group, but not in the off-pump group. The mean urinary NOx/Cr excretion ratio was significantly (P<0.01) higher in the off-pump group (0.51± 0.26 μmol/mg) than in the on-pump group (0.38± 0.20 μmol/mg) on day two. The mean serum CRP concentration was also significantly (P <0.01) higher in the off-pump group than in the on-pump group on day two. There was no significant difference in the mean cardiac index or the mean systemic vascular resistance index between the two groups after surgery. The mean serum CK-MB concentration was significantly (P<0.05) lower in the off-pump group than in the on-pump group on days one and two. These findings suggest that endogenous NO production is stimulated by a surgical inflammatory response and that the cardiopulmonary bypass procedure per se is not the inciting stimulus for NO production in patients undergoing CABG.

Enhanced expression of inducible nitric oxide synthase without vasodilator effect in chronically infected lungs

1999 ◽  
Vol 277 (3) ◽  
pp. L616-L627 ◽  
Author(s):  
Elaine Cadogan ◽  
Natalie Hopkins ◽  
Shay Giles ◽  
John G. Bannigan ◽  
John Moynihan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Vascular Resistance ◽  
Inos Expression ◽  
No Production ◽  
Inos Activity ◽  
Enhanced Expression ◽  
The Mean ◽  
Isolated Lungs ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

We hypothesized that abnormal ventilation-perfusion matching in chronically infected lungs was in part due to excess nitric oxide (NO) production after upregulation of inducible NO synthase (iNOS) expression. Rats were anesthetized and inoculated intratracheally with Pseudomonas aeruginosa incorporated into agar beads (chronically infected) or with sterile agar beads (placebo inoculated) and killed 10–15 days later. Immunohistochemistry demonstrated increased expression of iNOS and reduced expression of endothelial NOS (eNOS) in chronically infected compared with placebo-inoculated or noninoculated lungs. In isolated lungs from chronically infected rats, NOS inhibition with N ω-nitro-l-arginine methyl ester increased the mean perfusion pressure (14.4 ± 2.7 mmHg) significantly more than in the placebo-inoculated (4.8 ± 1.0 mmHg) or noninoculated (5.3 ± 0.8 mmHg) lungs ( P < 0.01). Although the chronically infected lungs were more sensitive to NOS inhibition, further evidence suggested that the increased iNOS expression was not associated with enhanced iNOS activity. Selective inhibitors of iNOS did not produce an increase in vascular resistance similar to that produced by nonselective inhibitors. Accumulation of nitrate/nitrite in the perfusate of isolated lungs was unchanged by chronic infection. Thus although iNOS expression was increased in chronic pulmonary infection, iNOS activity in the intact lung was not. Nonetheless, endogenous NO production was essential to maintain normal vascular resistance in these lungs.

scholarly journals Effect of nebulised l- and d-arginine on exhaled nitric oxide in steroid naive asthma

Thorax ◽  
2001 ◽  
Vol 56 (8) ◽  
pp. 602-606
Author(s):  
D C Chambers ◽  
J G Ayres
Keyword(s):  
Nitric Oxide ◽  
Area Under The Curve ◽  
Forced Expiratory Volume ◽  
No Production ◽  
Exhaled No ◽  
The Mean ◽  
Human Airways ◽  
Oxide Synthase ◽  
Blind Manner ◽  
Single Blind

BACKGROUNDNitric oxide (NO) is a product of the enzyme nitric oxide synthase (NOS) and is found in normal and asthmatic human airways. The administration ofl-arginine results in an increase in airway NO production in asthmatic subjects. This is thought to occur becausel-arginine is the substrate for NOS. However, studies in the systemic vasculature suggest that other mechanisms may be responsible.METHODSEight patients with steroid naive asthma each received 2.5 g l-arginine, 2.5 g d-arginine, and 2.0% saline by ultrasonic nebuliser on separate days in a randomised, single blind manner. Exhaled NO was measured by chemiluminescence and spirometric tests were performed before and for 3 hours after each administration. The mean concentration of NO after exposure was calculated from the area under the curve.RESULTSl-arginine,d-arginine, and 2.0% saline induced a mean (95% CI) maximal bronchoconstriction of 11.9% (–1.7 to 25.4), 10.0% (2.8 to 17.2), and 8.5% (–2.5 to 19.5) of the starting forced expiratory volume in one second (FEV1), respectively. Exhaled NO declined in proportion to the degree of bronchoconstriction (r=0.60, p<0.01). Bronchoconstriction and the acute reduction in exhaled NO resolved within 15 minutes. The mean post-exposure concentration of NO was 15.75 parts per billion (ppb) after l-arginine, 15.16 ppb after d-arginine, and 12.74 ppb after 2.0% saline. The mean (95% CI) difference between l-arginine and placebo was 3.01 (0.32 to 5.7) ppb, between d-arginine and placebo 2.42 (0.10 to 4.74) ppb, and between l- and d-arginine 0.59 (–1.56 to 2.74) ppb.CONCLUSIONSExhaled NO decreased with acute bronchoconstriction and returned to baseline with the resolution of bronchoconstriction. Exhaled NO increased following the administration of both l-arginine andd-arginine. Since NOS is stereospecific, this finding suggests that the increase in exhaled NO is not entirely mediated through an increase in NOS enzyme activity. We suggest that arginine may react in a non-stereospecific fashion with reactive oxygen species present in asthmatic airways.

scholarly journals Chemiluminescent measurements of nitric oxide pulmonary diffusing capacity and alveolar production in humans

2001 ◽  
Vol 91 (5) ◽  
pp. 1931-1940 ◽  
Author(s):  
Irene B. Perillo ◽  
Richard W. Hyde ◽  
Albert J. Olszowka ◽  
Anthony P. Pietropaoli ◽  
Lauren M. Frasier ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Breath Holding ◽  
No Production ◽  
Diffusing Capacity ◽  
Volume Changes ◽  
Pulmonary Diffusing Capacity ◽  
Single Breath ◽  
Coefficients Of Variation ◽  
Oxygen Tensions ◽  
Single Constant

Measurements of nitric oxide (NO) pulmonary diffusing capacity (Dl NO) multiplied by alveolar NO partial pressure (Pa NO) provide values for alveolar NO production (V˙a NO). We evaluated applying a rapidly responding chemiluminescent NO analyzer to measure Dl NO during a single, constant exhalation (DexNO) or by rebreathing (DrbNO). With the use of an initial inspiration of 5–10 parts/million of NO with a correction for the measured NO back pressure, DexNO in nine healthy subjects equaled 125 ± 29 (SD) ml · min−1 · mmHg−1 and DrbNO equaled 122 ± 26 ml · min−1 · mmHg−1. These values were 4.7 ± 0.6 and 4.6 ± 0.6 times greater, respectively, than the subject's single-breath carbon monoxide diffusing capacity (DsbCO). Coefficients of variation were similar to previously reported breath-holding, single-breath measurements of DsbCO. Pa NOmeasured in seven of the subjects equaled 1.8 ± 0.7 mmHg × 10−6 and resulted in V˙a NO of 0.21 ± 0.06 μl/min using DexNO and 0.20 ± 0.6 μl/min with DrbNO. DexNO remained constant at end-expiratory oxygen tensions varied from 42 to 682 Torr. Decreases in lung volume resulted in falls of DexNO and DrbNO similar to the reported effect of volume changes on DsbCO. These data show that rapidly responding chemiluminescent NO analyzers provide reproducible measurements of Dl NO using single exhalations or rebreathing suitable for measuring V˙a NO.

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