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1. |
Editorial Note |
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Respiration,
Volume 64,
Issue 1,
1997,
Page 1-1
H. Herzog,
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ISSN:0025-7931
DOI:10.1159/000196634
出版商:S. Karger AG
年代:1997
数据来源: Karger
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2. |
Central Sleep Apnea |
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Respiration,
Volume 64,
Issue 1,
1997,
Page 2-9
S. Thalhofer,
P. Dorow,
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PDF (1820KB)
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摘要:
A central apnea is a disorder characterized by apneic events during sleep with no associated ventilatory effort. Central sleep apnea syndrome is characterized by repeated apneas during sleep resulting from loss of respiratory effort. Although the etiology of central apnea remains obscure in most cases, current investigations into breathing control system during sleep and association with certain diseases have pointed out possible mechanisms. Ventilation during sleep is highly dependent on the nonbehavioral control system. As a result, any diseases affecting this control system could influence the breathing patterns while the patient is asleep. As our results show, most patients with central sleep apnea and without congestive heart failure had quantifiable abnormalities like diminished carbon dioxide response curves. Neurological diseases affecting the brainstem are able to produce breathing pattern disorders in sleep. Well-known neurological diseases such as arteriosclerosis in the elderly, infarctions, tumors, hemorrhage, accidents with damage of this region, encephalitis, poliomyelitis or other infectious diseases may cause central apnea during sleep, even if in wakefulness no abnormalities of breathing patterns are present. Apneas cause hypoxemia, hypercapnia and increased sympathicotonia. This may result in development of pulmonary artery hypertension or systemic hypertension. Published results demonstrate that medical treatment is ineffective in these patients. Implantation of a diaphragm pacing device is an invasive measure, the efficacy of the diphragm pacing has not been proven by long-term trials, however. Mechanical ventilation was shown to be the most efficient treatment. A therapeutic procedure using a timed n-BiPAP device is able to normalize blood gases during sleep. The n-BiPAP prevented the development of severe pulmonary artery hypertension during sleep.
ISSN:0025-7931
DOI:10.1159/000196635
出版商:S. Karger AG
年代:1997
数据来源: Karger
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3. |
Foreword |
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Respiration,
Volume 64,
Issue 1,
1997,
Page 3-4
Heinrich Matthys,
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PDF (294KB)
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ISSN:0025-7931
DOI:10.1159/000196727
出版商:S. Karger AG
年代:1997
数据来源: Karger
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4. |
History of Clinical Research on the Sleep Apnea Syndrome |
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Respiration,
Volume 64,
Issue 1,
1997,
Page 5-10
Wolfgang Kuhl,
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PDF (1175KB)
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摘要:
This article gives a brief historical overview of the literature on the sleep apnea syndrome (SAS), including initial case reports of the Pickwickian syndrome and its treatment with tracheostomy. It also highlights the beginnings of early clinical neurophysiology and describes the breakthrough in the understanding of the pathophysiology of SAS by performing polysomnography.
ISSN:0025-7931
DOI:10.1159/000196728
出版商:S. Karger AG
年代:1997
数据来源: Karger
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5. |
Long-Term Augmentation Therapy in Twenty Patients with Severe Alpha-1-Antitrypsin Deficiency – Three-Year Follow-Up |
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Respiration,
Volume 64,
Issue 1,
1997,
Page 10-15
Martin Schwaiblmair,
Claus Vogelmeier,
Günter Fruhmann,
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摘要:
The purpose of this uncontrolled, prospective study was to evaluate the influence of long-term augmentation therapy with plasma-derived α1-antitrypsin (AAT) on lung function parameters in patients with severe emphysema caused by AAT deficiency. Twenty patients (mean age 48 years) received AAT infusions once weekly for up to 36 months. No adverse effects were observed. At the beginning of the study, mean ( ± SEM) FEV1 was 1.35 ± 0.12 liters and mean TLco was 54 ± 4% of predicted. After 36 months of treatment, mean FEV1 was 1.25 ± 0.12 liters (p = n.s.) and the TLco was 52 ± 4% predicted (p = n.s.). Similar values were obtained before and after therapy for FVC (2.79 ± 0.23 vs. 2.82 ± 0.21 liters), MEF50 (0.72 ± 0.09 vs. 0.68 ± 0.08 liters/s), RV (4.60 ± 0.44 vs 4.45 ± 0.31 1) and TLC (7.72 ± 0.49 vs. 7.38 ± 0.42 1). The calculated annual loss of FEV1 (35.6 ml/year) was smaller than in historical untreated patients with A
ISSN:0025-7931
DOI:10.1159/000196636
出版商:S. Karger AG
年代:1997
数据来源: Karger
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6. |
Heavy Snorer Disease: From Snoring to the Sleep Apnea Syndrome – An Overview |
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Respiration,
Volume 64,
Issue 1,
1997,
Page 11-14
Elio Lugaresi,
Giuseppe Plazzi,
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PDF (778KB)
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摘要:
This short review discusses the clinical, pathophysiological and epidemiological aspects of heavy snorer disease. Snoring and obstructive apneas constitute the end points of the same syndrome, i.e. an enhancement in upper airway resistance during sleep. Obstructive apneas, and possibly snoring, are risk factors of chronic arterial hypertension.
ISSN:0025-7931
DOI:10.1159/000196730
出版商:S. Karger AG
年代:1997
数据来源: Karger
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7. |
How Important Is the Differentiation between Apnea and Hypopnea? |
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Respiration,
Volume 64,
Issue 1,
1997,
Page 15-21
Dieter Köhler,
Bernd Schönhofer,
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PDF (1657KB)
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摘要:
Apnea and hypopnea during sleep are often viewed as different expressions of the same sleep-related breathing disorder. In our point of view, both symptoms are two different entities which can occur in the same patient. We discuss the hypothesis that sleep apnea is a disorder associated with recurrent arousals and chronic activation of the sympathetic nervous system, leading to daytime sleepiness and disturbances in the autonomic system. Hypoventilation results from reduced alveolar ventilation and is associated with hypercapnia. In rare cases it is caused by genuine disorders of the breathing center, like Odine’s curse. In most cases, hypoventilation is secondary to an underlying disease and a strategy of the body, to avoid respiratory muscle failure. Treatment trials of hypoventilation of the respiratory muscles by stimulating the breathing center failed to be benefical. However, unloading treatment with long-term oxygen and/or home mechanical ventilation improves arterial blood gases, physical activity and prognosi
ISSN:0025-7931
DOI:10.1159/000196731
出版商:S. Karger AG
年代:1997
数据来源: Karger
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8. |
Beta-2-Agonists Have Antioxidant Function in vitro. 1. Inhibition of Superoxide Anion, Hydrogen Peroxide, Hypochlorous Acid and Hydroxyl Radical |
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Respiration,
Volume 64,
Issue 1,
1997,
Page 16-22
Adrian Gillissen,
Malgorzata Jaworska,
Birgit Schärling,
Dominique van Zwoll,
Gerhard Schultze-Werninghaus,
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摘要:
β2-Agonists are known to have anti-inflammatory efficacy. In this context, β2-agonists are also capable of inhibiting oxidant production of cultured inflammatory cells. As the mechanisms of this function still remain speculative, the purpose of this study was to quantify the efficacy of β2-agonists in vitro to inhibit superoxide anion (O2-), hydrogen peroxide (H2O2), hydroxyl radical (OH•) and hypochlorous acid (HOCl). We tested the following antiasthma drugs: ipratropium bromide, salbutamol (salbutamol base), fenoterol (fenoterol hydrobromide), terbutaline (terbutaline sulfate), isoproterenol, prednisolone (prednisolone hydrogensuccinate), beclomethasone (beclomethasone dipropionate) and theophylline (theophylline sulfate). Antioxidant function was quantified by using the following assay systems: O2- (ferricytochrome c + xanthine/xanthine oxidase), H2O2 (phenol red + 5·• 10-6M H2O2 OH• (deoxyribose assay) and HOCl (HOCl/OCl- in luminol-dependent chemiluminescence). At 10-4M, the anti- H2O2 and anti- O2- capacity was as follows: salbutamol/terbutaline < fenoterol < isoproterenol. All β2-agonists (10-4M 50% (p < 0.01). In contrast, moderate OH• reduction (10-30%) by the β2-agonists is regarded as an nonspecific effect, due to the high concentrations needed (10-3M). Corticosteroids and theophylline had no antioxidant effect. These results demonstrate the different redox potentials of different phenol types within the molecular structure of the β2-agonists. The good antioxidative function of isoproterenol is related to ortho formation of the phenol ring, whereas fenoterol has two phenol rings which can be oxidized. A direct oxidant scavenger function may explain the ability of β2-agonists to reduce the oxidant production of inflammatory
ISSN:0025-7931
DOI:10.1159/000196637
出版商:S. Karger AG
年代:1997
数据来源: Karger
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9. |
Sympathetic Activity and Blood Pressure in the Sleep Apnea Syndrome |
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Respiration,
Volume 64,
Issue 1,
1997,
Page 22-28
Eugene C. Fletcher,
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PDF (1335KB)
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ISSN:0025-7931
DOI:10.1159/000196732
出版商:S. Karger AG
年代:1997
数据来源: Karger
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10. |
Beta-2-Agonists Have Antioxidant Function in vitro. 2. The Effect of Beta-2-Agonists on Oxidant-Mediated Cytotoxicity and on Superoxide Anion Generated by Human Polymorphonuclear Leukocytes |
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Respiration,
Volume 64,
Issue 1,
1997,
Page 23-28
Adrian Gillissen,
Doris Wickenburg,
Dominique van Zwoll,
Gerhard Schultze-Werninghaus,
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PDF (1353KB)
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摘要:
Therapeutic agents which may be able to enhance the antioxidant screen of the epithelial surface of the lung have the potential to influence the progression of lung inflammation. This study evaluates the efficacy of a variety of antiasthma drugs to reduce oxidant-mediated cytotoxicity and to inhibit superoxide anion generated by human polymorphonuclear leukocytes. We quantified in vitro the prevention of H2O2-mediated cytotoxicity (lactate dehydrogenase release assay) using the antiasthma drugs as follows: ipratropium bromide, salbutamol (salbutamol base), fenoterol (fenoterol hydrobromide), terbutaline (terbutaline sulfate), isoproterenol, prednisolone (prednisolone hydrogensuccinate), beclomethasone (17,21-beclomethasone dipropionate) and reduced glutathione. Furthermore, fenoterol and isoproterenol were evaluated ex vivo to reduce superoxide anion (O2-) generated by freshly isolated polymorphonuclear cells (PMN) from smokers with chronic obstructive lung disease (n = 10). Using a concentration of 10-4M, reduction of cytotoxicity was quite different among β2 ipratropium bromide (18.1%). Corticosteroids and theophylline had no antioxidant effect. The cellular O2- production of freshly isolated PMN was significantly (p < 0.05, comparisons 0 vs. ≧ 10-7M) reduced with fenoterol and isoproterenol at concentrations ≧ 10-7M. Propranolol had no inhibitory effect on antioxidant properties of β2-agonists. We hypothesize that the antioxidant function of β2-agonists is related to the number and formation of hydroxyl groups of the phenol rings within their molecular structure. These results demonstrate that β2-agonists have in part a good intrinsic scavenger function on reactive oxygen species when used in micromolar concentrations. However, to achieve this effect supratherapeutic concentrations were necessary. Thus, the conceivable benefit of β2-agonists in the treatment of high oxidant burden in vivo seems
ISSN:0025-7931
DOI:10.1159/000196638
出版商:S. Karger AG
年代:1997
数据来源: Karger
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