Endothelin-1 levels in the pathophysiology of chronic obstructive pulmonary disease and bronchial asthma

Spiropoulos, Kostas; Trakada, Georgia; Nikolaou, E.; Prodromakis, E.; Efremidis, G; Pouli, A.; Koniavitou, A.

doi:10.1016/s0954-6111(03)00129-x

Cited by 39 publications

(36 citation statements)

References 35 publications

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“…Levels of ET-1 were increased in CS and CH groups, consistent with the increased levels observed in smokers and COPD patients [29,30]. However, no differences in ET-1 levels were observed in CSCH animals, suggesting that the synergistic effect on Ppa does not appear to be mediated by ET-1 in plasma.…”

Section: Discussionsupporting

confidence: 80%

Effects of cigarette smoke and hypoxia on pulmonary circulation in the guinea pig

Ferrer¹,

Peinado²,

Castañeda³

et al. 2011

Eur Respir J

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Cigarette smoke (CS) and chronic hypoxia (CH) can produce pulmonary hypertension. Similarities and differences between both exposures and their interaction have not been explored. The aim of the present study was to investigate the effects of CS and CH, as single factors or in combination, on the pulmonary circulation in the guinea pig.51 guinea pigs were exposed to CS for 12 weeks and 32 were sham-exposed. 50% of the animals in each group were additionally exposed to CH for the final 2 weeks. We measured pulmonary artery pressure (Ppa), and the weight ratio between the right ventricle (RV) and left ventricle plus the septum. Pulmonary artery contractility in response to noradrenaline (NA), endothelium-dependent vasodilatation and distensibility were evaluated in organ bath chambers. The number of small intrapulmonary vessels showing immunoreactivity to smooth muscle (SM) a-actin and double elastic laminas was assessed microscopically.CS and CH induced similar increases of Ppa and RV hypertrophy (p,0.05 for both), effects that were further enhanced when both factors were combined. CH increased the contractility to NA (p,0.01) and reduced the distensibility (p,0.05) of pulmonary arteries. Animals exposed to CS showed an increased number of small vessels with positive immunoreactivity to SM a-actin (p,0.01) and those exposed to CH a greater proportion of vessels with double elastic laminas (p,0.05).We conclude that CH amplifies the detrimental effects of CS on the pulmonary circulation by altering the mechanical properties of pulmonary arteries and enhancing the remodelling of pulmonary arterioles.KEYWORDS: Chronic obstructive pulmonary disease, cigarette smoke, hypoxia, pulmonary hypertension, vascular remodelling P ulmonary hypertension is a common and serious complication of chronic obstructive pulmonary disease (COPD). It is considered to result from the effects of chronic hypoxaemia on pulmonary vessels. Indeed, acute and chronic exposure to hypoxia results in smooth muscle cell (SMC) and adventitial fibroblast proliferation [1]. Nevertheless, structural changes in the pulmonary arteries of COPD patients differ from those observed in subjects exposed to a hypoxic environment. Whereas subjects living at high altitudes show medial hypertrophy, COPD patients show prominent changes in the intima [2]. Intimal hypertrophy is present in nonhypoxaemic COPD patients and in smokers with normal lung function, suggesting that vascular changes may be triggered by cigarette smoke (CS) before hypoxaemia develops.Cigarette smoking is associated with endothelial dysfunction [3], increased expression of growth factors [4] and inflammatory cell infiltrate in pulmonary arteries [5]. These factors may induce SMC proliferation and increase pulmonary vascular resistance. The molecular mechanisms by which CS induces vascular changes remain unknown, but they might be related to oxidative damage [6].The effects of hypoxia on human lungs are difficult to characterise because it is usually related to the presence of primary lu...

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Section: Discussionsupporting

confidence: 80%

Effects of cigarette smoke and hypoxia on pulmonary circulation in the guinea pig

Ferrer¹,

Peinado²,

Castañeda³

et al. 2011

Eur Respir J

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“…Among a wide range of phlogogenic molecules affecting the development of systemic inflammation in COPD one should also mention the vasoactive mediator ET-1 [30]. The results of this study showed an increase in the level of this peptide in all COPD patients compared to the reference group.…”

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confidence: 48%

The Significance of Soluble Molecules of Cellular Adhesion, Nitric Oxide Metabolites, and Endothelin-1 and Their Associations as Markers of Progression of Inflammation in COPD

Kubysheva¹,

Postnikova²,

Soodaeva³

et al. 2017

Sovrem Tehnol Med

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The aim of the investigation was to assess the significance of the content of metabolites of the nitric oxide, sICAM-1 and sICAM-3 in blood serum and in exhaled breath condensate, the serum level of endothelin-1 as systemic and topical markers of inflammation in patients with COPD, and their correlations with the parameters of lung ventilation function. Materials and Methods. 91 patients with COPD, aged from 46 to 67, and 21 healthy, non-smoking volunteers took part in the study. The material for investigation was blood serum and exhaled breath condensate.Results. The severity of progression of COPD was linked with an increase in the serum content of sCD50, sCD54, ET-1, as well as in the concentrations of metabolites of nitric oxide in blood and in exhaled breath condensate. For the patients with COPD we determined the associations between the function of pulmonary ventilation and the levels of ET-1, sICAM-1, sICAM-3 and the value of ΣNO 2 -/NO 3 -. The resulting correlations between the concentration of soluble adhesion molecules, the values of nitrosative stress, and ET-1 level indicate that they are involved in the genesis of chronic inflammation in COPD patients.Key words: chronic obstructive pulmonary disease; COPD; endothelin-1; ET-1; nitrosative stress; soluble molecules of adhesion ICAM-1 and ICAM-3; exhaled breath condensate. Markers of progression of inflammation in COpDThe steady increase in the prevalence of chronic obstructive pulmonary disease (COPD) and the mortality rate associated with this pathology indicate the importance of studying the pathogenic mechanisms of development of this disease [1]. The identification of new activity markers and the progression of inflammation are key tasks in the studies of these mechanisms.The result of the immune-mediated mechanisms of inflammation in response to damaging factors is the excessive migration of effector cells to the

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“…Plasma ET-1 concentrations are also elevated in COPD patients, particularly in patients who develop nocturnal hypoxemia during the night (Trakada et al, 2001;Spiropoulos et al, 2003) and in patients with hypoxemia (Faller et al, 1998), but it is not correlated with secondary pulmonary hypertension (Bacakoglu et al, 2003). This may reflect the release of ET-1 by hypoxemia, suggesting that the release of ET-1 may contribute to pulmonary vasoconstriction and pulmonary hypertension in COPD patients.…”

Section: Formationmentioning

confidence: 99%

Mediators of Chronic Obstructive Pulmonary Disease

2004

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Endothelin-1 levels in the pathophysiology of chronic obstructive pulmonary disease and bronchial asthma

Cited by 39 publications

References 35 publications

Effects of cigarette smoke and hypoxia on pulmonary circulation in the guinea pig

Effects of cigarette smoke and hypoxia on pulmonary circulation in the guinea pig

The Significance of Soluble Molecules of Cellular Adhesion, Nitric Oxide Metabolites, and Endothelin-1 and Their Associations as Markers of Progression of Inflammation in COPD

Mediators of Chronic Obstructive Pulmonary Disease

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