NO: COPD and beyond

Jones, Andrew; Evans, Timothy W.

doi:10.1136/thx.52.2008.s16

Cited by 20 publications

(8 citation statements)

References 50 publications

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“…Der Einsatz von Vasodilatatoren unter Einschluss von NO hat bisher enttäuschende Ergebnisse gezeigt. So kann inhaliertes NO den Gasaustausch bei Patienten mit Hypoxämie infolge von Ventilations-/Perfusions-Inhomogenitäten verschlechtern [183,184]. Daher ist NO bei Patienten mit stabiler COPD kontraindiziert.…”

Section: Vasodilatatorenunclassified

Leitlinie zur Diagnostik und Therapie von Patienten mit chronisch obstruktiver Bronchitis und Lungenemphysem (COPD)

et al. 2018

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This document is a revision of the guideline for diagnosis and treatment of COPD that replaces the version from 2007. A multitude of recent reports regarding risk factors, diagnosis, assessment, prevention and pharmacological as well as non-pharmacological treatment options made a major revision mandatory. The new guideline is based on the GOLD document taking into account specifics in Germany and Austria.

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Section: Vasodilatatorenunclassified

Leitlinie zur Diagnostik und Therapie von Patienten mit chronisch obstruktiver Bronchitis und Lungenemphysem (COPD)

et al. 2018

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“…Vasodilators: Vasodilators (hydralazine, nitrates, nifedipine, verapamil, diltiazem, angiotensin‐converting enzyme [ACE] inhibitors) do not produce sustained relief of pulmonary hypertension in patients with COPD 86 , 87 . They can worsen oxygenation (by increasing blood flow through poorly ventilated lung) and result in systemic hypotension.…”

Section: Hypoxaemia and Pulmonary Hypertensionmentioning

confidence: 99%

“…Some vasodilators (eg, calcium antagonists) have been shown to reduce right ventricular pressure with minimal side effects and increased well‐being, at least in the short term. Nitric oxide worsens V/Q mismatching and is therefore contraindicated in patients with COPD 86 , 87 …”

Section: Hypoxaemia and Pulmonary Hypertensionmentioning

confidence: 99%

The COPDX Plan: Australian and New Zealand Guidelines for the management of Chronic Obstructive Pulmonary Disease 2003

McKenzie

Frith

2003

Medical Journal of Australia

155

221

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“…In addition, vascular smooth muscle tone is increased, as evidenced by acute reduction in pulmonary arterial pressure in response to vasodilatory agents (16,27,32). For patients with chronic obstructive pulmonary disease, these hypoxia-induced structural and functional changes in the pulmonary vasculature correlate with the development of pulmonary hypertension and increased mortality.…”

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confidence: 99%

HIF-1 regulates hypoxic induction of NHE1 expression and alkalinization of intracellular pH in pulmonary arterial myocytes

Shimoda¹,

Fallon²,

Pisarcik³

et al. 2006

American Journal of Physiology-Lung Cellular and Molecular Phys

184

178

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. HIF-1 regulates hypoxic induction of NHE1 expression and alkalinization of intracellular pH in pulmonary arterial myocytes. Am J Physiol Lung Cell Mol Physiol 291: L941-L949, 2006. First published June 9, 2006 doi:10.1152/ajplung.00528.2005.-Vascular remodeling resulting from altered pulmonary arterial smooth muscle cell (PASMC) growth is a contributing factor to the pathogenesis of hypoxic pulmonary hypertension. PASMC growth requires an alkaline shift in intracellular pH (pHi) and we previously showed that PASMCs isolated from mice exposed to chronic hypoxia exhibited increased Na ϩ /H ϩ exchanger (NHE) expression and activity, which resulted in increased pHi. However, the mechanism by which hypoxia caused these changes was unknown. In this study we tested the hypothesis that hypoxia-induced changes in PASMC pH homeostasis are mediated by the transcriptional regulator hypoxiainducible factor 1 (HIF-1). Consistent with previous results, increased NHE isoform 1 (NHE1) mRNA and protein, enhanced NHE activity, and an alkaline shift in pHi were observed in PASMCs isolated from wild-type mice exposed to chronic hypoxia (3 wk at 10% O2). In contrast, these changes were absent in PASMCs isolated from chronically hypoxic mice with partial deficiency for HIF-1. Exposure of PASMCs to hypoxia ex vivo (48 h at 4% O2) or overexpression of HIF-1 in the absence of hypoxia also increased NHE1 mRNA and protein expression. Our results indicate that full expression of HIF-1 is essential for hypoxic induction of NHE1 expression and changes in PASMC pH homeostasis and suggest a novel mechanism by which HIF-1 mediates pulmonary vascular remodeling during the pathogenesis of hypoxic pulmonary hypertension.hypoxia-inducible factor 1; pulmonary arterial smooth muscle cell

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NO: COPD and beyond

Abstract: Background. Inhalation of nitric oxide (NO) causes selective pulmonary vasodilation and improves arterial oxygenation in acute respiratory (Lancet 1996;347:436-40)

Cited by 20 publications

References 50 publications

Leitlinie zur Diagnostik und Therapie von Patienten mit chronisch obstruktiver Bronchitis und Lungenemphysem (COPD)

Leitlinie zur Diagnostik und Therapie von Patienten mit chronisch obstruktiver Bronchitis und Lungenemphysem (COPD)

The COPDX Plan: Australian and New Zealand Guidelines for the management of Chronic Obstructive Pulmonary Disease 2003

HIF-1 regulates hypoxic induction of NHE1 expression and alkalinization of intracellular pH in pulmonary arterial myocytes

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