Basal and induced NO formation in the pharyngo-oral tract influences estimates of alveolar NO levels

2009 ◽  
Vol 106 (2) ◽  
pp. 513-519 ◽  
Author(s):  
Andrei Malinovschi ◽  
Christer Janson ◽  
Lena Holm ◽  
Lennart Nordvall ◽  
Kjell Alving
Keyword(s):  
Nitric Oxide ◽  
Healthy Subjects ◽  
Fold Increase ◽  
Peripheral Inflammation ◽  
Flow Rates ◽  
Axial Diffusion ◽  
Dietary Nitrate ◽  
No Formation ◽  
Nitrate Load ◽  
Nitrate And Nitrite

The present study analyzed how models currently used to distinguish alveolar from bronchial contribution to exhaled nitric oxide (NO) are affected by manipulation of NO formation in the pharyngo-oral tract. Exhaled NO was measured at multiple flow rates in 15 healthy subjects in two experiments: 1) measurements at baseline and 5 min after chlorhexidine (CHX) mouthwash and 2) measurements at baseline, 60 min after ingestion of 10 mg NaNO3/kg body wt, and 5 min after CHX mouthwash. Alveolar NO concentration (CalvNO) and bronchial flux (J′awNO) were calculated by using the slope-intercept model with or without adjustment for trumpet shape of airways and axial diffusion (TMAD). Salivary nitrate and nitrite were measured in the second experiment. CalvNO [median (range)] was reduced from 1.16 ppb (0.77, 1.96) at baseline to 0.84 ppb (0.57, 1.48) 5 min after CHX mouthwash ( P < 0.001). The TMAD-adjusted CalvNO value after CHX mouthwash was 0.50 ppb (0, 0.85). The nitrate load increased J′awNO from 32.2 nl/min (12.2, 60.3) to 57.1 nl/min (22.0, 119) in all subjects and CalvNO from 1.47 ppb (0.73, 1.95) to 1.87 ppb (10.85, 7.20) in subjects with high nitrate turnover (>10-fold increase of salivary nitrite after nitrate load). CHX mouthwash reduced CalvNO levels to 1.15 ppb (0.72, 2.07) in these subjects with high nitrate turnover. All these results remained consistent after TMAD adjustment. We conclude that estimated alveolar NO concentration is affected by pharyngo-oral tract production of NO in healthy subjects, with a decrease after CHX mouthwash. Moreover, unknown ingestion of dietary nitrate could significantly increase estimated alveolar NO in subjects with high nitrate turnover, and this might be falsely interpreted as a sign of peripheral inflammation. These findings were robust for TMAD.

A simple technique to characterize proximal and peripheral nitric oxide exchange using constant flow exhalations and an axial diffusion model

2007 ◽  
Vol 102 (1) ◽  
pp. 417-425 ◽  
Author(s):  
Peter Condorelli ◽  
Hye-Won Shin ◽  
Anna S. Aledia ◽  
Philip E. Silkoff ◽  
Steven C. George
Keyword(s):  
Nitric Oxide ◽  
Diffusion Model ◽  
Healthy Subjects ◽  
Elimination Rate ◽  
Compartment Model ◽  
No Production ◽  
Constant Flow ◽  
Axial Diffusion ◽  
Common Technique ◽  
Airway Tree

The most common technique employed to describe pulmonary gas exchange of nitric oxide (NO) combines multiple constant flow exhalations with a two-compartment model (2CM) that neglects 1) the trumpet shape (increasing surface area per unit volume) of the airway tree and 2) gas phase axial diffusion of NO. However, recent evidence suggests that these features of the lungs are important determinants of NO exchange. The goal of this study is to present an algorithm that characterizes NO exchange using multiple constant flow exhalations and a model that considers the trumpet shape of the airway tree and axial diffusion (model TMAD). Solution of the diffusion equation for the TMAD for exhalation flows >100 ml/s can be reduced to the same linear relationship between the NO elimination rate and the flow; however, the interpretation of the slope and the intercept depend on the model. We tested the TMAD in healthy subjects ( n = 8) using commonly used and easily performed exhalation flows (100, 150, 200, and 250 ml/s). Compared with the 2CM, estimates (mean ± SD) from the TMAD for the maximum airway flux are statistically higher ( J′awNO = 770 ± 470 compared with 440 ± 270 pl/s), whereas estimates for the steady-state alveolar concentration are statistically lower (CANO = 0.66 ± 0.98 compared with 1.2 ± 0.80 parts/billion). Furthermore, CANO from the TMAD is not different from zero. We conclude that proximal (airways) NO production is larger than previously predicted with the 2CM and that peripheral (respiratory bronchioles and alveoli) NO is near zero in healthy subjects.

scholarly journals A Narrative Review on Dietary Strategies to Provide Nitric Oxide as a Non-Drug Cardiovascular Disease Therapy: Beetroot Formulations—A Smart Nutritional Intervention

Foods ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 859
Author(s):  
Diego dos Santos Baião ◽  
Davi Vieira Teixeira da Silva ◽  
Vania Margaret Flosi Paschoalin
Keyword(s):  
Nitric Oxide ◽  
Patient Adherence ◽  
Biological Fluids ◽  
Bioactive Compound ◽  
Nutritional Intervention ◽  
Gene Expressions ◽  
Dietary Nitrate ◽  
Metabolic Functions ◽  
Nitrate And Nitrite ◽  
Dietary Strategies

Beetroot is a remarkable vegetable, as its rich nitrate and bioactive compound contents ameliorate cardiovascular and metabolic functions by boosting nitric oxide synthesis and regulating gene expressions or modulating proteins and enzyme activities involved in these cellular processes. Dietary nitrate provides a physiological substrate for nitric oxide production, which promotes vasodilatation, increases blood flow and lowers blood pressure. A brief narrative and critical review on dietary nitrate intake effects are addressed herein by considering vegetable sources, dosage, intervention regimen and cardioprotective effects achieved in both healthy and cardiovascular-susceptible individuals. Compared to other nitrate-rich vegetables, beets were proven to be the best choice for non-drug therapy because of their sensorial characteristics and easy formulations that facilitate patient adherence for long periods, allied to bioaccessibility and consequent effectiveness. Beets were shown to be effective in raising nitrate and nitrite in biological fluids at levels capable of promoting sustained improvement in primary and advanced hemodynamic parameters.

Intraluminal generation of nitric oxide from dietary nitrate is maximal at the gastro-oesophageal junction

2001 ◽  
Vol 120 (5) ◽  
pp. A245-A245
Author(s):  
E HENY ◽  
K IIJIMA ◽  
A MORIYA ◽  
K MCELROY ◽  
J GRANT ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Dietary Nitrate

scholarly journals NO formation by a catalytically self-sufficient bacterial nitric oxide synthase from Sorangium cellulosum

2009 ◽  
Vol 106 (38) ◽  
pp. 16221-16226 ◽  
Author(s):  
T. Agapie ◽  
S. Suseno ◽  
J. J. Woodward ◽  
S. Stoll ◽  
R. D. Britt ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Sorangium Cellulosum ◽  
No Formation ◽  
Oxide Synthase

scholarly journals Natural Product Nitric Oxide Chemistry: New Activity of Old Medicines

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Hong Jiang ◽  
Ashley C. Torregrossa ◽  
Deepa K. Parthasarathy ◽  
Nathan S. Bryan
Keyword(s):  
Nitric Oxide ◽  
Conventional Medicine ◽  
Herbal Medicines ◽  
Cost Effective ◽  
Preventative Care ◽  
Current State ◽  
No Bioavailability ◽  
Reported Health ◽  
Nitrate And Nitrite ◽  
Care Measure

The use of complementary and alternative medicine (CAM) as a therapy and preventative care measure for cardiovascular diseases (CVD) may prove to be beneficial when used in conjunction with or in place of conventional medicine. However, the lack of understanding of a mechanism of action of many CAMs limits their use and acceptance in western medicine. We have recently recognized and characterized specific nitric oxide (NO) activity of select alternative and herbal medicines that may account for many of their reported health benefits. The ability of certain CAM to restore NO homeostasis both through enhancing endothelial production of NO and by providing a system for reducing nitrate and nitrite to NO as a compensatory pathway for repleting NO bioavailability may prove to be a safe and cost-effective strategy for combating CVD. We will review the current state of science behind NO activity of herbal medicines and their effects on CVD.

The influence of acupuncture on salivary flow rates in healthy subjects

1997 ◽  
Vol 24 (3) ◽  
pp. 204-208 ◽  
Author(s):  
I. DAWIDSON ◽  
M. BLOM ◽  
T. LUNDEBERG ◽  
B. ANGMAR-MÅNSSON
Keyword(s):  
Healthy Subjects ◽  
Salivary Flow ◽  
Flow Rates

Abstract 442: Endoplasmic Reticulum (ER) Stress in the Subfornical Organ (SFO) Induces Peripheral Inflammation in Angiotensin II (Ang-II)-dependent Hypertension

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Heinrich E Lob ◽  
Jiunn Song ◽  
Scott D Butler ◽  
Allyn L Mark ◽  
Robin L Davisson
Keyword(s):  
T Cell ◽  
Er Stress ◽  
T Cell Activation ◽  
Cell Activation ◽  
Adaptive Immune Response ◽  
Fold Increase ◽  
Peripheral Inflammation ◽  
Ang Ii ◽  
Peripheral Vascular ◽  
Control Virus

The SFO is implicated in peripheral T cell activation and the genesis of Ang-II-dependent hypertension. Our recent studies show that ER stress in the SFO is also a key mechanism underlying the development of Ang-II hypertension. Because the ER is closely integrated with initiation of the adaptive immune response, we hypothesized that ER stress in the SFO contributes to peripheral inflammation in Ang-II hypertension. First, 5 days of intracerebroventricular (ICV) infusion of thapsigargin (Tg, 1 ug/day), a chemical ER stress inducer, caused a significant increase in CD3 + T cells in aortas (Tg: 11.9 ± 3.5 x 10 3 cells/aorta vs. Vehicle: 2.2 ± 0.7 x 10 3 cells/aorta , n = 6, p<0.05) and blood (Tg: 9.9 ± 1.8 x 10 4 cells/ mL vs. Vehicle: 2.9 ± 0.6 x 10 4 cells/ mL, n = 6, p<0.05). Furthermore, quantitative real-time PCR of SFO micropunches showed a 15-fold increase of TNF-α, a pro-inflammatory cytokine, a 3-fold increase of CCL5, a T cell attracting chemokine and a 3-fold increase in CD3, a T cell marker, (n = 4, p<0.05). To test the functional role of ER stress in the SFO in peripheral T cell activation, we targeted an adenovirus encoding GRP78 (AdGRP78), a molecular ER stress inhibitor, to this brain region during chronic systemic Ang-II infusion (600 ng/kg/min, 14 days). Our results demonstrate a significant reduction in T cell accumulation in aortas compared to control virus (AdLacZ) treatment (AdGRP78: 0.5 ± 0.07 x 10 4 cells/aorta vs. AdLacZ: 8.7 ± 2.1 x 10 4 cells/aorta, n = 6, p<0.05). These data show that 1) brain ER stress induces inflammation in the SFO and peripheral vascular T cell activation, and 2) ER stress in the SFO is linked to peripheral vascular T cell activation in Ang-II-dependent hypertension. These results suggest that ER stress and inflammation in the SFO induce peripheral vascular T cell activation and inflammation in Ang-II hypertension.

Endothelial microparticles increase in mitral valve disease and impair mitral valve endothelial function

2013 ◽  
Vol 304 (7) ◽  
pp. E695-E702 ◽  
Author(s):  
Hong-Bo Ci ◽  
Zhi-Jun Ou ◽  
Feng-Jun Chang ◽  
Dong-Hong Liu ◽  
Guo-Wei He ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Mitral Valve ◽  
Mitral Regurgitation ◽  
Mitral Valve Disease ◽  
Healthy Subjects ◽  
Heat Shock Protein 90 ◽  
Valve Disease ◽  
No Production ◽  
Endothelial Microparticles

Mitral valve endothelial cells are important for maintaining lifelong mitral valve integrity and function. Plasma endothelial microparticles (EMPs) increased in various pathological conditions related to activation of endothelial cells. However, whether EMPs will increase in mitral valve disease and their relationship remains unclear. Here, 81 patients with mitral valve disease and 45 healthy subjects were analyzed for the generation of EMPs by flow cytometry. Human mitral valve endothelial cells (HMVECs) were treated with EMPs. The phosphorylation of Akt and endothelial nitric oxide synthase (eNOS), the association of eNOS and heat shock protein 90 (HSP90), and the generation of nitric oxide (NO) and superoxide anion (O2˙−) were measured. EMPs were increased significantly in patients with mitral valve disease compared with those in healthy subjects. EMPs were negatively correlated with mitral valve area in patients with isolated mitral stenosis. EMPs were significantly higher in the group with severe mitral regurgitation than those in the group with mild and moderate mitral regurgitation. Furthermore, EMPs were decreased dramatically in both Akt and eNOS phosphorylation and the association of HSP90 with eNOS in HMVECs. EMPs decreased NO production but increased O2˙− generation in HMVECs. Our data demonstrated that EMPs were significantly increased in patients with mitral valve disease. The increase of EMPs can in turn impair HMVEC function by inhibiting the Akt/eNOS-HSP90 signaling pathway. These findings suggest that EMPs may be a therapeutic target for mitral valve disease.

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