Nitric oxide exhalation correlates with ventilatory response to exercise in patients with heart disease

Adachi, Hitoshi; Sakurai, Shigeki; Toyama, Takuji; Hara, Hiroshi; Taniguchi, Koichi; Ito, Haruki

doi:10.1016/s1388-9842(03)00107-7

Cited by 11 publications

(12 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Katz et al have investigated the impaired NO production in heart failure and a similar result was supported by other reports. [26][27][28] In contrast, several reports demonstrated the increase of NO production. [29][30][31] If NO production is increased in heart failure, NO might be produced by the increase of iNOS, which is upregulated by several cytokines due to development of heart failure.…”

Section: Discussionmentioning

confidence: 89%

Repeated Sauna Therapy Increases Arterial Endothelial Nitric Oxide Synthase Expression and Nitric Oxide Production in Cardiomyopathic Hamsters

Ikeda

Biro

Kamogawa

et al. 2005

Circ J

View full text Add to dashboard Cite

n patients with chronic heart failure (CHF), vascular resistance is increased through the activation of neurohumoral systems, such as the sympathetic nervous, renin-angiotensin and endothelin systems. 1 Vascular endothelial function, which is mainly represented by endothelium-dependent vasodilatory function through the production of vasodilators derived from the endothelium such as nitric oxide (NO), prostacyclin and endothelium-derived hyperpolarizing factors, is impaired in CHF and affects clinical symptoms. 2-5 Impaired vascular endothelial function leads to increased vascular tone and vascular remodeling, which reduces peripheral blood flow and oxygen delivery to the skeletal muscles, followed by progressive exercise intolerance and clinical symptoms. [2][3][4][5] Therapies that improve endothelial function, such as angiotensin-converting enzyme inhibitors and regular exercise, improve the clinical symptoms and prognosis in CHF. [6][7][8][9] We reported that sauna therapy at 60°C induces vasodilation of the systemic and pulmonary arteries and veins, reduces cardiac preload and afterload and improves hemodynamics, clinical symptoms and cardiac arrythmia in patients with CHF. [10][11][12] We also clarified that the beneficial effects of sauna therapy for CHF are caused by improved vascular endothelial function and the normalizing of the neurohormonal systems. 13 Furthermore, we showed that repeated sauna therapy improved the survival of cardiomyopathic hamsters with CHF. 14 Vascular endothelial dysfunction in CHF is mainly due to decreased NO production induced by decreased levels of endothelial NO synthase (eNOS) expression and increased oxidative stress. [15][16][17] We have already reported that repeated sauna therapy increased arterial eNOS protein and mRNA expressions from the normal levels in healthy hamsters. 18 However, it is important to determine whether repeated sauna therapy could increase eNOS expression downregulated by CHF. The present study aims to investigate whether repeated sauna therapy modulates eNOS expression and NO production in CHF. Methods AnimalsWe used male TO-2 cardiomyopathic hamsters (Bio Breeders, Fitchburg, MA, USA) as a model of clinical dilated cardiomyopathy. These animals develop CHF (characterized by symptoms such as general edema and pleural effusion) at around 30 weeks of age and die within a year. 19,20 Male Syrian golden hamsters (Japan SLC, Hamamatsu, Japan) served as normal controls. All animals Background Vascular endothelial dysfunction is involved in the pathophysiology of chronic heart failure (CHF). It has been reported that sauna therapy, which allows thermal vasodilation, improves vascular endothelial dysfunction in patients with CHF. The present study investigates the mechanisms through which sauna therapy improves endothelial dysfunction induced by CHF. Methods and ResultsNormal control and male TO-2 cardiomyopathic hamsters were used. Thirty-week-old TO-2 hamsters were treated daily with an experimental far infrared-ray dry sauna system for 15 min at 39°C f...

show abstract

Section: Discussionmentioning

confidence: 89%

Repeated Sauna Therapy Increases Arterial Endothelial Nitric Oxide Synthase Expression and Nitric Oxide Production in Cardiomyopathic Hamsters

Ikeda

Biro

Kamogawa

et al. 2005

Circ J

View full text Add to dashboard Cite

show abstract

“…4,40,49 -52 Increased mortality risk in association with decreased exhaled NO production could be related to autonomic dysregulation of ventilation during exercise, progression of right ventricular dysfunction in response to increased pulmonary vascular resistance, or other hemodynamic factors associated with decreased aerobic capacity. 41,47,48,53 Interpretation of our findings is potentially limited by several considerations. Although our findings with 2 biomarkers of endothelial function and subsequent mortality risk are internally consistent in our study cohorts, the observational nature of the study does not allow one to draw conclusions regarding a causal link between endothelial dysfunction and mortality, because unmeasured confounders may have contributed to the observed associations.…”

Section: Discussionmentioning

confidence: 93%

“…[37][38][39][40] Increased exhaled NO production in response to exercise may be attributed to increased shear stress-induced release of NO from alveolar endothelial cells and increased exercise hyperventilationdependent mass transport of NO from alveoli. 11,41,42 Airway inflammation may also contribute to exhaled NO production. 36,43,44 In patients with CHF, decreased exhaled NO production during exercise is associated with increased pulmonary vascular resistance and decreased maximal aerobic capacity.…”

Section: Discussionmentioning

confidence: 99%

“…36,43,44 In patients with CHF, decreased exhaled NO production during exercise is associated with increased pulmonary vascular resistance and decreased maximal aerobic capacity. 41,[45][46][47][48] Decreased exhaled NO production in patients with CHF may be attributed to decreased diffusion/transport of NO from lower-airway sources and/or a reduced rate of cellular production of NO in the lower respiratory tract. 4,40,49 -52 Increased mortality risk in association with decreased exhaled NO production could be related to autonomic dysregulation of ventilation during exercise, progression of right ventricular dysfunction in response to increased pulmonary vascular resistance, or other hemodynamic factors associated with decreased aerobic capacity.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Vascular Endothelial Dysfunction and Mortality Risk in Patients With Chronic Heart Failure

et al. 2005

View full text Add to dashboard Cite

Background-Endothelial function is known to be impaired in subjects with chronic heart failure (CHF), but the association between endothelial function and subsequent mortality risk in CHF has not been previously reported. Methods and Results-Biomarkers of endothelial function in the systemic arterial circulation (flow-mediated dilation [FMD] in the brachial artery) and the pulmonary circulation (exhaled nitric oxide [NO] production during submaximal exercise) were prospectively assessed in 259 subjects with New York Heart Association class II-III CHF. In subjects with FMD measurements (nϭ149), there were 12 deaths and 5 urgent transplantations over a median follow-up period of 841 days. In subjects with exhaled NO production measurements (nϭ110), there were 18 deaths and 1 urgent transplantation over a median follow-up period of 396 days. Both decreased FMD and decreased exhaled NO production were associated with increased risk of death or urgent transplantation after adjustment for other known CHF prognostic

show abstract

“…E/ !CO2 become greater. 11,12) In addition, when the volume of the pulmonary arterial perfusion is small, or the amount of carbon dioxide in the pulmonary arterial flow becomes smaller, the partial pressure of alveolar CO2 (PACO2) diminishes. Since end-tidal gas primarily consists of alveolar gas, PETCO2 is equal to PACO2.…”

Section: Significance Of Each Parametermentioning

confidence: 99%

Cardiopulmonary Exercise Test

Adachi

2017

Int. Heart J.

Self Cite

View full text Add to dashboard Cite

SummaryThe cardiopulmonary exercise test (CPX) is an essential examination for detecting pathophysiological derangement and determining treatment policy because it clarifies not only the changes of hemodynamics but also abnormality in the whole body during exercise where heart disease patients often feel symptoms.To utilize CPX effectively, we must understand each parameter, such as peak oxygen uptake (peak !O2), peak !O2/HR, and !E/ !CO2. In addition, comparison of each parameter, for example, peak !O2 and !E/ !CO2, and peak!O2 and peak!O2/HR, is useful to detect the pathophysiological abnormalities.In this article, I will describe how CPX should be used in clinical settings. (Int Heart J 2017; 58: 654-665)

show abstract

Nitric oxide exhalation correlates with ventilatory response to exercise in patients with heart disease

Cited by 11 publications

References 27 publications

Repeated Sauna Therapy Increases Arterial Endothelial Nitric Oxide Synthase Expression and Nitric Oxide Production in Cardiomyopathic Hamsters

Repeated Sauna Therapy Increases Arterial Endothelial Nitric Oxide Synthase Expression and Nitric Oxide Production in Cardiomyopathic Hamsters

Vascular Endothelial Dysfunction and Mortality Risk in Patients With Chronic Heart Failure

Cardiopulmonary Exercise Test

Contact Info

Product

Resources

About