PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 11404867

Chronic obstructive pulmonary disease.

N M Foley
View original source ↗Export metadata ↓

Abstract

COPD is the most common chronic condition in the UK and it varies in severity from mild through to disabling and severe disease with respiratory failure. The treatment of the disease is tailored to the severity of the symptoms and the cornerstones are stopping smoking, inhaled bronchodilator and inhaled corticosteroid therapy. Preoperative assessment of patients with COPD needs to be thorough; remember that these patients may have concomitant ischaemic heart disease. Patients with severe COPD are at particularly high risk when given intravenous sedatives, opiates or general anaesthetics.

Explore related subjects

Adrenergic beta-AgonistsAdultAgedBronchitisBronchodilator AgentsDental Care for Chronically IllFemaleForced Expiratory VolumeGlucocorticoidsHumansLung Diseases, ObstructiveMaleMiddle AgedOxygen Inhalation TherapyPeak Expiratory Flow RatePrevalencePulmonary Diffusing CapacityPulmonary EmphysemaRespiratory InsufficiencyRisk FactorsSmoking CessationUnited KingdomVital CapacityJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

N M Foley. 2000. Chronic obstructive pulmonary disease.. https://pubmed.ncbi.nlm.nih.gov/11404867/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Orchidectomy increases beta-adrenoceptor activation-mediated neuronal nitric oxide and noradrenaline release in rat mesenteric artery.

BACKGROUND/AIMS: A previous study has demonstrated that endogenous male sex hormones do not alter neuronal nitric oxide (NO) release in rat mesenteric artery. However, the regulatory role of endogenous male sex hormones on noradrenaline (NA) release in rat mesenteric artery is not known. The present study was designed to analyze whether endogenous male sex hormones influence the NA release induced by electrical field stimulation (EFS), as well as the possible modification in NA and neuronal NO release by presynaptic beta-adrenoceptor activation. METHODS: For this purpose, mesenteric arteries from control and orchidectomized male Sprague-Dawley rats were used. Basal and EFS-induced neuronal NO and NA release, as well as the contractile effect induced by EFS, was measured. RESULTS: Basal and EFS-induced neuronal NO and NA release were similar in arteries from control and orchidectomized rats. The beta-adrenoceptor agonist clenbuterol did not modify EFS-induced neuronal NO and NA release in arteries from control rats. In contrast, in arteries from orchidectomized animals, clenbuterol increased both neuronal NO and NA release; this increase was prevented by incubation with the beta-adrenoceptor antagonist propranolol. However, the contractile response elicited by EFS was not modified by clenbuterol in either group of rats. CONCLUSIONS: These results show that orchidectomy does not alter the EFS-induced NA release. What is more, activation of presynaptic beta-adrenoceptors does not modify EFS-induced NA and neuronal NO release in arteries from control rats although it increases the release of both neurotransmitters in arteries from orchidectomized rats. Despite these modifications, the EFS-induced contractile response is preserved in arteries from orchidectomized rats.

Adrenergic beta-Agonists↗
PubMed2007

Effect of formoterol and salmeterol on IL-6 and IL-8 release in airway epithelial cells.

Beta(2)-adrenoceptors are widely distributed and occur on airway epithelial cells. The aim of this study was to find out whether the two long-acting beta(2)-agonists formoterol and salmeterol influence interleukin-6 (IL-6) and -8 (IL-8) release from airway epithelial cells in vitro. A549 cells and primary bronchial epithelial cells (PBEC) were stimulated with organic dust from pig barns. Non-stimulated and dust-stimulated cells were incubated for 24h with formoterol or salmeterol (10(-13)-10(-6)M) and the release of IL-6 and IL-8 into the medium was assessed by ELISA technique. Propranolol (10(-5)M) or sotalol (10(-3)M) were used to block the beta(2)-agonist mediated effects. Formoterol and salmeterol both induced enhancement of IL-6 and IL-8 release and added to the effect of organic dust. This enhanced release was blocked by a beta-blocker in PBEC but not in A549 cells. To our knowledge, this is the first time beta(2)-agonists have been shown to stimulate IL-6 release from airway epithelial cells. The results indicate different mechanisms of beta(2)-agonist action in bronchial and alveolar epithelial cells. Furthermore, our results indicate that A549 cells do not possess functional beta(2)-adrenoceptors.

Adrenergic beta-Agonists↗