Andreas, Stefan

[["dc.bibliographiccitation.artnumber","7"],["dc.bibliographiccitation.journal","Respiratory Research"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Luethje, Lars"],["dc.contributor.author","Raupach, Tobias"],["dc.contributor.author","Michels, Hellmuth"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Koegler, Harald"],["dc.contributor.author","Andreas, Stefan"],["dc.date.accessioned","2017-09-07T11:47:34Z"],["dc.date.available","2017-09-07T11:47:34Z"],["dc.date.issued","2009"],["dc.description.abstract","Background: Systemic effects of chronic obstructive pulmonary disease (COPD) significantly contribute to severity and mortality of the disease. We aimed to develop a COPD/emphysema model exhibiting systemic manifestations of the disease. Methods: Female NMRI mice were treated 5 times intratracheally with porcine pancreatic elastase (emphysema) or phosphate-buffered saline (control). Emphysema severity was quantified histologically by mean linear intercept, exercise tolerance by treadmill running distance, diaphragm dysfunction using isolated muscle strips, pulmonary hypertension by measuring right ventricular pressure, and neurohumoral activation by determining urinary norepinephrine concentration. Results: Mean linear intercept was higher in emphysema (260.7 +/- 26.8 mu m) than in control lungs (24.7 +/- 1.7 mu m). Emphysema mice lost body weight, controls gained weight. Running distance was shorter in emphysema than in controls. Diaphragm muscle length was shorter in controls compared to emphysema. Fatigue tests of muscle strips revealed impaired relaxation in emphysema diaphragms. Maximum right ventricular pressure and norepinephrine were elevated in emphysema compared to controls. Linear correlations were observed between running distance changes and intercept, right ventricular weight, norepinephrine, and diaphragm length. Conclusion: The elastase mouse model exhibited severe emphysema with consecutive exercise limitation, and neurohumoral activation. The model may deepen our understanding of systemic aspects of COPD."],["dc.identifier.doi","10.1186/1465-9921-10-7"],["dc.identifier.gro","3143160"],["dc.identifier.isi","000263727200001"],["dc.identifier.pmid","19175913"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13854"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/643"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1465-9921"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Exercise intolerance and systemic manifestations of pulmonary emphysema in a mouse model"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","273"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","European Journal of Heart Failure"],["dc.bibliographiccitation.lastpage","280"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Luethje, Lars"],["dc.contributor.author","Renner, Bernd"],["dc.contributor.author","Kessels, Roger"],["dc.contributor.author","Vollmann, Dirk"],["dc.contributor.author","Raupach, Tobias"],["dc.contributor.author","Gerritse, Bart"],["dc.contributor.author","Tasci, Selcuk"],["dc.contributor.author","Schwab, Joerg O."],["dc.contributor.author","Zabel, Markus"],["dc.contributor.author","Zenker, Dieter"],["dc.contributor.author","Schott, Peter"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Unterberg-Buchwald, Christina"],["dc.contributor.author","Andreas, Stefan"],["dc.date.accessioned","2017-09-07T11:47:31Z"],["dc.date.available","2017-09-07T11:47:31Z"],["dc.date.issued","2009"],["dc.description.abstract","Aims The combined therapeutic impact of atrial overdrive pacing (ACIP) and cardiac resynchronization therapy (CRT) on central steep apnoea (CSA) in chronic heart failure (CHF) so far has not been investigated. We aimed to evaluate the effect of CRT alone and CRT + AOP on CSA in CHF patients and to compare the influence of CRT on CHF between CSA positive and CSA negative patients. Methods and results Thirty patients with CRT indication underwent full night polysomnography, echocardiography, exercise testing, and neurohumoral evaluation before and 3 months after CRT implantation. In CSA positive patients (60%), two additional steep studies were conducted after 3 months of CRT, with CRT alone or CRT + ACIP, in random order. Cardiac resynchronization therapy resulted in significant improvements of NYHA class, left ventricular ejection fraction, N-terminal pro-brain natriuretic peptide, VO(2)max, and quality of life irrespective of the presence of CSA. Cardiac resynchronization therapy also reduced the central apnoea-hypopnoea index (AHI) (33.6 +/- 14.3 vs. 23.8 +/- 16.9 h(-1); P < 0.01) and central apnoea index (17.3 +/- 14.1 vs. 10.9 +/- 13.9 h(-1); P < 0.01) without altering steep stages. Cardiac resynchronization therapy with atrial overdrive pacing resulted in a small but significant additional decrease of the central AHI (23.8 +/- 16.9 vs. 21.5 +/- 16.9 h(-1); P < 0.01). Conclusion In this study, CRT significantly improved CSA without altering sleep stages. Cardiac resynchronization therapy with atrial. overdrive pacing resulted in a significant but minor additional improvement of CSA. Positive effects of CRT were irrespective of the presence of CSA."],["dc.identifier.doi","10.1093/eurjhf/hfn042"],["dc.identifier.gro","3143143"],["dc.identifier.isi","000265845700008"],["dc.identifier.pmid","19147446"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/625"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: Bakken Research Center, Maastricht, Netherlands"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","1388-9842"],["dc.title","Cardiac resynchronization therapy and atrial overdrive pacing for the treatment of central sleep apnoea"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","589"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","COPD: Journal of Chronic Obstructive Pulmonary Disease"],["dc.bibliographiccitation.lastpage","594"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Haarmann, Helge"],["dc.contributor.author","Folle, Jan"],["dc.contributor.author","Xuan Phuc Nguyen, Xuan Phuc Nguyen"],["dc.contributor.author","Herrmann, Peter"],["dc.contributor.author","Heusser, Karsten"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Andreas, Stefan"],["dc.contributor.author","Raupach, Tobias"],["dc.date.accessioned","2017-09-07T11:54:43Z"],["dc.date.available","2017-09-07T11:54:43Z"],["dc.date.issued","2016"],["dc.description.abstract","Exercise intolerance, skeletal muscle dysfunction, and reduced daily activity are central in COPD patients and closely related to quality of life and prognosis. Studies assessing muscle exercise have revealed an increase in sympathetic outflow as a link to muscle hypoperfusion and exercise limitation. Our primary hypothesis was that muscle sympathetic nerve activity (MSNA) correlates with exercise limitation in COPD. MSNA was evaluated at rest and during dynamic or static handgrip exercise. Additionally, we assessed heart rate, blood pressure, CO2 tension, oxygen saturation (SpO(2)), and breathing frequency. Ergospirometry was performed to evaluate exercise capacity. We assessed MSNA of 14 COPD patients and 8 controls. In patients, MSNA was negatively correlated with peak oxygen uptake (VO2 % pred) (r = -0.597; p = 0.040). During dynamic or static handgrip exercise, patients exhibited a significant increase in MSNA, which was not observed in the control group. The increase in MSNA during dynamic handgrip was highly negatively correlated with peak exercise capacity in Watts (w) and peak oxygen uptake (VO2/kg) (r = -0.853; p = 0.002 and r = -0.881; p = 0.002, respectively). Our study reveals an association between increased MSNA and limited exercise capacity in patients with COPD. Furthermore, we found an increased sympathetic response to moderate physical exercise (handgrip), which may contribute to exercise intolerance in COPD."],["dc.identifier.doi","10.3109/15412555.2015.1136272"],["dc.identifier.gro","3141749"],["dc.identifier.isi","000381997300009"],["dc.identifier.pmid","26829234"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/646"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Taylor & Francis Inc"],["dc.relation.eissn","1541-2563"],["dc.relation.issn","1541-2555"],["dc.title","Sympathetic Activation is Associated with Exercise Limitation in COPD"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","199"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.lastpage","204"],["dc.bibliographiccitation.volume","70"],["dc.contributor.author","Raupach, Tobias"],["dc.contributor.author","Shahab, Lion"],["dc.contributor.author","Neubert, Karin"],["dc.contributor.author","Felten, Dorothea"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Andreas, Stefan"],["dc.date.accessioned","2017-09-07T11:48:47Z"],["dc.date.available","2017-09-07T11:48:47Z"],["dc.date.issued","2008"],["dc.description.abstract","Objective: This study assessed a newly set-up, hospital-based smoking cessation clinic with regard to continuous abstinence rates and the effectiveness of concomittant nicotine replacement therapy. Methods: Smoking status of 369 participants of this 8-week cognitive-behavioural smoking cessation group programme was obtained using exhaled carbon monoxide at the end of the course as well as self-report 6 months after the course. In addition to demographic data, FTND score, SDS score, and usage of nicotine replacement products were recorded. Results: Overall, 29.8% of all participants reported to have been continuously abstinent for 6 months after the course. Success rates increased significantly during the first year after initiation of the programme (from 15 to 35%, p < 0.001), indicating a learning process of the staff running the course. Nicotine replacement therapy was used by 51.3% of participants, but 58% of these discontinued its use within 5 weeks. Nicotine substitution for more than 5 weeks was associated with a 50% success rate after 6 months. Conclusions: Our data indicate a learning effect of smoking cessation course staff and a possible minimum duration required for nicotine replacement to be effective. Practice implications: The observed learning effect in smoking cessation programmes should be considered when evaluating newly established interventions of this kind. Patients tend to stop nicotine replacement therapy too early, thereby decreasing their chances of middle-term abstinence. (C) 2007 Elsevier Ireland Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.pec.2007.10.005"],["dc.identifier.gro","3143356"],["dc.identifier.isi","000253270900008"],["dc.identifier.pmid","18031972"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/861"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Ireland Ltd"],["dc.publisher.place","Clare"],["dc.relation.conference","4th International Conference on Shared Decision Making"],["dc.relation.eventlocation","Freiburg, GERMANY"],["dc.relation.ispartof","Patient Education and Counseling"],["dc.relation.issn","0738-3991"],["dc.title","Implementing a hospital-based smoking cessation programme: Evidence for a learning effect"],["dc.type","conference_paper"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","European Respiratory Journal"],["dc.bibliographiccitation.volume","42"],["dc.contributor.author","Haarmann, Helge"],["dc.contributor.author","Folle, Jan"],["dc.contributor.author","Andreas, Stefan"],["dc.contributor.author","Raupach, Tobias"],["dc.date.accessioned","2018-11-07T09:21:01Z"],["dc.date.available","2018-11-07T09:21:01Z"],["dc.date.issued","2013"],["dc.identifier.isi","000209370404317"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29017"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","European Respiratory Soc Journals Ltd"],["dc.publisher.place","Sheffield"],["dc.relation.issn","1399-3003"],["dc.relation.issn","0903-1936"],["dc.title","Sympathetic activation is related to exercise limitation in COPD"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","215"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Pulmonary Pharmacology & Therapeutics"],["dc.bibliographiccitation.lastpage","220"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Raupach, Tobias"],["dc.contributor.author","Luethje, Lars"],["dc.contributor.author","Koegler, Harald"],["dc.contributor.author","Duve, Christian"],["dc.contributor.author","Schweda, Frank"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Andreas, Stefan"],["dc.date.accessioned","2017-09-07T11:44:19Z"],["dc.date.available","2017-09-07T11:44:19Z"],["dc.date.issued","2011"],["dc.description.abstract","Objectives: COPD with emphysema causes marked neurohumoral activation. Angiotensin II receptors are highly expressed within the lung and interfere with mechanisms involved in the progression of emphysema. This study examined the effects of an angiotensin II receptor blocker (ARB) on pulmonary and systemic manifestations of emphysema in a mouse model. Methods: Female NMRI mice received five intratracheal instillations of porcine pancreatic elastase (emphysema; n = 11) or phosphate-buffered saline (PBS; n = 4). Emphysema severity was quantified histologically by mean linear intercept, exercise tolerance by treadmill running distance, and lung biomechanics by compliance. Following emphysema induction, 6 mice were treated with the ARB irbesartan for 8 weeks, while 5 mice receiving standard food served as controls. Results: Following emphysema induction, mean linear intercept was higher in elastase-treated than in PBS-treated lungs (103.0 +/- 6.2 mu m vs. 35.0 +/- 0.6 mu m; p = 0.043) while running distance was shorter in emphysema mice (418.6 +/- 83.5 m vs. 906.6 +/- 244.6 m, p = 0.028). Irbesartan-treated emphysema mice showed a lower mean linear intercept (90.8 +/- 3.8 mu m vs. 121.5 +/- 8.1 mu m; p = 0.005), improved compliance (163.6 +/- 55.9 mu l/cmH(2)O vs. 354.4 +/- 72.5 mu l/cmH(2)O; p = 0.063) and greater running distance (p ANOVA = 0.015) compared to emphysema mice receiving standard food. Conclusions: The ARB irbesartan elicits encouraging beneficial effects on emphysema severity, lung biomechanics and exercise capacity in an emphysema mouse model. These findings might help to understand the corresponding positive effects of angiotensin II receptor blockade noticed in patients with COPD. (C) 2010 Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.pupt.2010.12.006"],["dc.identifier.gro","3142753"],["dc.identifier.isi","000289396400006"],["dc.identifier.pmid","21187155"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/192"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: Sanofi-Aventis (formerly Sanofi-Synthelabo), Paris, France"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Academic Press Ltd- Elsevier Science Ltd"],["dc.relation.issn","1094-5539"],["dc.title","Local and systemic effects of angiotensin receptor blockade in an emphysema mouse model"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","46"],["dc.bibliographiccitation.journal","BMC Pulmonary Medicine"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Haarmann, Helge"],["dc.contributor.author","Mohrlang, Cordula"],["dc.contributor.author","Tschiesner, Uta"],["dc.contributor.author","Rubin, David B."],["dc.contributor.author","Bornemann, Thore"],["dc.contributor.author","Rueter, Karin"],["dc.contributor.author","Bonev, Slavtcho"],["dc.contributor.author","Raupach, Tobias"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Andreas, Stefan"],["dc.date.accessioned","2017-09-07T11:44:26Z"],["dc.date.available","2017-09-07T11:44:26Z"],["dc.date.issued","2015"],["dc.description.abstract","Background: Neurohumoral activation is present in COPD and might provide a link between pulmonary and systemic effects, especially cardiovascular disease. Because long acting inhaled beta-agonists reduce hyperinflation, they could reduce sympathoexcitation by improving the inflation reflex. We aimed to evaluate if inhaled therapy with salmeterol reduces muscle sympathetic nerve activity (MSNA) evaluated by microneurography. Methods: MSNA, heart rate, blood pressure, and respiration were continually measured. After baseline recording of 20 minutes, placebo was administered; after further 45 minutes salmeterol (50 mu g) was administered which was followed by a further 45 minutes of data recording. Additionally, lung function, plasma catecholamine levels, arterial pulse wave velocity, heart rate variability, and baroreflex sensitivity were evaluated. Following 4 weeks of treatment with salmeterol 50 mu g twice daily, measurements were repeated without placebo administration. Results: A total of 32 COPD patients were included. Valid MSNA signals were obtained from 18 patients. Change in MSNA (bursts/100 heart beats) following acute administration of salmeterol did not differ significantly from the change following placebo (-1.96 +/- 9.81 vs. -0.65 +/- 9.07; p = 0.51) although hyperinflation was significantly reduced. Likewise, no changes in MSNA or catecholamines were observed after 4 weeks. Heart rate increased significantly by 3.8 +/- 4.2 (p < 0.01) acutely and 3.9 +/- 4.3 bpm (p < 0.01) after 4 weeks. Salmeterol treatment was safe and well tolerated. Conclusions: By using microneurography as a gold standard to evaluate sympathetic activity we found no change in MSNA following salmeterol inhalation. Thus, despite an attenuation of hyperinflation, the long acting beta-agonist salmeterol does not appear to reduce nor incite sympathoexcitation."],["dc.identifier.doi","10.1186/s12890-015-0054-7"],["dc.identifier.gro","3141919"],["dc.identifier.isi","000356211900001"],["dc.identifier.pmid","25924990"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12294"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2533"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: GlaxoSmithKline, Munich, Germany [SCO114520]"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1471-2466"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Inhaled beta-agonist does not modify sympathetic activity in patients with COPD"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","107"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Respiratory Medicine"],["dc.bibliographiccitation.lastpage","113"],["dc.bibliographiccitation.volume","104"],["dc.contributor.author","Raupach, Tobias"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Herrmann, Peter"],["dc.contributor.author","Luethje, Lars"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Andreas, Stefan"],["dc.date.accessioned","2017-09-07T11:46:44Z"],["dc.date.available","2017-09-07T11:46:44Z"],["dc.date.issued","2010"],["dc.description.abstract","Objectives: Neurohumoral. activation has been shown to be present in patients with chronic obstructive pulmonary disease (COPD). The increase in respiratory muscle work might be responsible for the observed elevation of sympathetic tone via a respiratory muscle ergoreflex in these patients. The aim of this study is to investigate whether moderately increasing inspiratory resistive loading will impact on sympathetic activity in healthy subjects and COPD patients. Methods: Efferent muscle sympathetic nerve activity, blood pressure, heart rate and respiratory movements were continuously measured in 15 patients and 15 healthy control subjects. In order to increase work of breathing as evaluated by the tension-time index, inspiratory resistive loading was performed white patients were breathing through a spirometer. Results: At baseline, sympathetic nerve activity was significantly elevated in patients. Resistive loading increased work of breathing (tension-time index) by roughly 110% (COPD) and 130% (controls) but did not significantly alter blood gases or sympathetic activity in either group. Conclusions: Doubting the work of breathing does not affect sympathetic activation in COPD patients or healthy control subjects. Thus in COPD the respiratory muscle ergoreflex does not seem to play a major rote in sympathoexcitation. (C) 2009 Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.rmed.2009.06.011"],["dc.identifier.gro","3143004"],["dc.identifier.isi","000274889300015"],["dc.identifier.pmid","19619996"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/471"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","W B Saunders Co Ltd"],["dc.relation.issn","0954-6111"],["dc.title","Inspiratory resistive loading does not increase sympathetic tone in COPD"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","386"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.lastpage","392"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Raupach, Tobias"],["dc.contributor.author","Schafer, K."],["dc.contributor.author","Konstantinides, Stavros V."],["dc.contributor.author","Andreas, S."],["dc.date.accessioned","2018-11-07T10:21:51Z"],["dc.date.available","2018-11-07T10:21:51Z"],["dc.date.issued","2006"],["dc.description.abstract","The evidence that active smoking is a risk factor for cardiovascular disease (CVD) and the leading cause of preventable death is overwhelming. However, numerous epidemiological findings indicate that even passive exposure to cigarette smoke may exert detrimental effects on vascular homoeostasis. Recent experimental data provide a deeper insight into the pathophysiological mechanisms linking secondhand smoke (SHS) to CVD. Importantly, most of these effects appear to be characterized by a rapid onset. For example, the relatively low doses of toxins inhaled by passive smoking are sufficient to elicit acute endothelial dysfunction, and these effects may be related, at least in part, to the inactivation of nitric oxide. Moreover, passive smoking may directly impair the viability of endothelial cells and reduce the number and functional activity of circulating endothelial progenitor cells. In addition, platelets of non-smokers appear to be susceptible to pro-aggregatory changes with every passive smoke exposure. Overall, SHS induces oxidative stress and promotes vascular inflammation. Apart from vascoconstriction and thrombus formation, however, the myocardial oxygen balance is further impaired by SHS-induced adrenergic stimulation and autonomic dysfunction. These data strongly suggest that passive smoking is capable of precipitating acute manifestations of CVD (atherothrombosis) and may also have a negative impact on the outcome of patients who suffer acute coronary syndromes."],["dc.identifier.doi","10.1093/eurheartj/ehi601"],["dc.identifier.isi","000235278100006"],["dc.identifier.pmid","16230308"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42169"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0195-668X"],["dc.title","Secondhand smoke as an acute threat for the cardiovascular system: a change in paradigm"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","276"],["dc.bibliographiccitation.issue","16"],["dc.bibliographiccitation.journal","Deutsches Ärzteblatt international"],["dc.bibliographiccitation.lastpage","U16"],["dc.bibliographiccitation.volume","106"],["dc.contributor.author","Andreas, Stefan"],["dc.contributor.author","Hering, Thomas"],["dc.contributor.author","Muehlig, Stephan"],["dc.contributor.author","Nowak, Dennis"],["dc.contributor.author","Raupach, Tobias"],["dc.contributor.author","Worth, Heinrich"],["dc.date.accessioned","2018-11-07T08:30:43Z"],["dc.date.available","2018-11-07T08:30:43Z"],["dc.date.issued","2009"],["dc.description.abstract","Background: As many as 50% of older smokers develop chronic obstructive pulmonary disease (COPD), and more than 80% of COPD-associated morbidity is caused by tobacco smoking. Despite the severe symptoms from which COPD patients suffer, they are often unable to quit smoking on their own. Methods: Experts from 9 medical societies, under the aegis of the German Society of Pulmonology and Respiratory Medicine (Deutsche Gesellschaft fur Pneumologie und Beatmungsmedizin), have developed an S3 guideline on smoking cessation in COPD. They took previously published guidelines into account, as well as more than 2000 initially surveyed publications, and created the new guideline in two consensus conferences followed by a Delphi process. Results: The following strongly evidence-based statements can be made: A smoking cessation strategy based on a combination of medication and psychosocial support has been found to be effective in COPD patients. Smoking cessation improves pulmonary function, alleviates dyspnea and cough, reduces the frequency of COPD exacerbations, and lowers mortality. Mere smoking reduction does not improve pulmonary function or alleviate symptoms. Smoking cessation is the most effective and least expensive single means of lowering the risk of developing COPD and of arresting its progression. Smoking cessation should therefore be strongly promoted at all levels of health care delivery. Conclusions: There is no question that smoking cessation ranks among the most effective medical interventions, yet the German health care system still does not assign it an adequate priority. Dtsch Arztebl Int 2009; 106(16): 276-82 DOI: 10.3238/arztebl.2009.0276"],["dc.description.sponsorship","German Society for Pneumology and Respiratory Medicine (DGP)"],["dc.identifier.doi","10.3238/arztebl.2009.0276"],["dc.identifier.isi","000268469800002"],["dc.identifier.pmid","19547629"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5816"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16959"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Deutscher Aerzte-verlag Gmbh"],["dc.relation.issn","1866-0452"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Smoking Cessation in Chronic Obstructive Pulmonary Disease An Effective Medical Intervention"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]