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T Köhnlein

Publications and source records attributed to T Köhnlein.

12 recordsLinked to original sources
PubMed2006

[Non-invasive ventilation].

Non-invasive ventilation is a technique to ventilate patients without endotracheal intubation and analgosedation. Pressure tight masks allow the ventilation of patients with severe respiratory or ventilatory insufficiency. Non-invasive ventilation may be used as short-term treatment for patients with acute ventilatory decompensation, as well as for long-term therapy at home for patients with chronic respiratory diseases. The typical indications are hypoxaemic respiratory failure in pneumonia or cardiogenic pulmonary edema, and hypercapnic ventilatory insufficiency in severe chronic obstructive pulmonary disease, neuromuscular disorders, or advanced kyphoscoliosis. The physiological background, technical aspects of performing non-invasive ventilation, and typical indications are discussed.

Continuous Positive Airway Pressure↗
PubMed2004

[Multicenter study on "non-invasive ventilation in patients with severe chronic obstructive pulmonary disease and emphysema(COPD)"].

Non-invasive ventilation is applied with increasing frequency in patients with chronic hypercapnic COPD and insufficiency of the ventilatory pump. In the few existing clinical trials on long-term use of NIV, no significant improvement on survival could be proven, mainly due to methodical reasons. The "National Task Force for Non-invasive ventilation and weaning" plans to study patients with severe COPD and hypercapnic ventilatory pump insufficiency in a prospective, randomised, multicentre clinical trial over one year. In the intervention group, NIV will be applied for at least six hours per day in addition to standard COPD-treatment. The target of mechanical ventilation is a reduction of PCO (2) during spontaneous breathing by at least 20 %, or into the normal range. The main outcome parameter is all-cause mortality, secondary outcome parameters are course of the disease, exercise capacity, quality of life and consumption of medical resources. The sample size is estimated on 300 patients (150 control group, 150 intervention group). The whole study will take approximately three years.

Emphysema↗
PubMed2002

Central sleep apnoea syndrome in patients with chronic heart disease: a critical review of the current literature.

The prevalence, prognosis, clinical presentation, pathophysiology, diagnosis, and treatment of the central sleep apnoea syndrome (CSAS) are reviewed and its relationship with congestive heart failure (CHF) is discussed. Adequately powered trials are needed with survival and health status as end points to establish whether correction of sleep related breathing abnormalities improves the outcome in patients with CHF.

Heart Failure↗
PubMed2002

Assisted ventilation for heart failure patients with Cheyne-Stokes respiration.

Patients with chronic congestive cardiac failure (CCF) frequently suffer from central sleep apnoea syndrome (CSAS). Continuous positive airway pressure (CPAP) has been suggested as a treatment. The authors hypothesised that bilevel ventilation might be easier to initiate and superior to CPAP at correcting the sleep-related abnormality of breathing in patients with CCF. After excluding those with a history suggestive of obstructive sleep apnoea, 35 patients with CCF (left ventricular ejection fraction <35%) were screened with overnight oximetry and the diagnosis of CSAS was established with polysomnography in 18. Two 14-day cycles of CPAP (0.85 kPa (8.5 mbar)) or bilevel ventilation (0.85/0.3 kPa (8.5/3 mbar)) in random order, were compared in a crossover study. Sixteen patients (13 males), mean age 62.0+/-7.4 yrs completed the study. The pretreatment apnoea/hypopnoea index of 26.7+/-10.7 was significantly reduced by CPAP and bilevel ventilation to 7.7+/-5.6 and 6.5+/-6.6, respectively. The arousal index fell from 31.1+/-10.0 per hour of sleep to 15.7+/-5.4 and 16.4+/-6.9, respectively. Significant and equal improvements with CPAP and bilevel ventilation were found for sleep quality, daytime fatigue, circulation time and New York Heart Association class. The authors conclude that continuous positive airway pressure and bilevel ventilation equally and effectively improve Cheyne-Stokes respiration in patients with congestive cardiac failure.

Adolescent↗
PubMed2001

[Heart failure and central respiratory dysregulation. Cheyne-Stokes respiration during sleep in advanced left heart failure].

Central sleep apnoea, especially Cheyne-Stokes respiration, is found in 45 to 66% of patients with congestive heart failure (CHF) in functional classes NYHA II to IV. Cheyne-Stokes breathing cycles are characterised by central apnoeas, followed by a crescendo--like increase of tidal volume into hyperventilation and a subsequent decline of tidal volume, ending in another central apnoea. Cheyne-Stokes respiration has been shown to be a poor prognostic factor for patients with CHF. Apnoeas and hypopnoeas cause marked oxygen desaturation and rises of carbon dioxide concentrations in the blood. The resumption of breathing is frequently associated with arousals, which might cause daytime symptoms like fatigue and sleepiness as well as persistent activation of the sympathetic nervous system. Elevated concentrations of catecholamines increase cardiac work, adversely affecting cardiac function. Serum catecholamines are known to augment the chemoreceptor susceptibility for carbon dioxide. This might be one reason for the permanent mild hyperventilation found in these patients during wakefulness. Increased chemoreceptor responsiveness destabilises the feedback control of breathing, and hyperventilation below the apnoeic threshold grows more likely. Other contributing factors for the development of Cheyne-Stokes respiration include alterations in the control of breathing during sleep and the increased circulation time between the lung and chemoreceptors in CHF patients. The feedback regulation of breathing might be less dampened since carbon dioxide levels are reduced in these patients. Treatment includes nCPAP, but in many cases this is poorly tolerated in patients with central sleep apnoea. Future approaches to Cheyne-Stokes respiration might focus on improving ventilatory pattern and pharmacological manipulation of carbon dioxide receptor susceptibility.

Arousal↗
PubMed2000

Evidence of a defective thiol status of alveolar macrophages from COPD patients and smokers. Chronic obstructive pulmonary disease.

In increasing numbers of pulmonary diseases an association with a loss of intracellular thiols, mainly glutathione, is postulated. Therefore, the quantitative measurement of thiols within different viable cells is a possible metabolic parameter for cellular function and defense capacity of all pulmonary immune cells including alveolar macrophages (AM), that are highly compromised by oxidative stress. In this study the cellular thiol content was determined using fluorochrom conjugated chloromethyl derivatives (5-chloromethylfluorescein diacetate, CMFDA) in flow cytometry. The procedure was evaluated in vitro using biochemical techniques for glutathione quantification. Based on this approach, AM obtained from bronchoalveolar lavage (BAL) of smokers and patients with chronic obstructive pulmonary disease (COPD) showed a significant thiol deficiency compared to a nonsmoker/non-COPD group. The cellular thiol expression of AM from smokers and COPD patients reached only 50 and 53% of the control group. Lowest thiol concentrations (47% of control) were detected within the smoker(+)/COPD(+) group. This intracellular thiol deficiency significantly correlated with reduced lung function (FEV(1), PaO(2)). With regard to the tightly regulated thiol metabolism of immune cells, these results imply the onset of functional disturbances in thiol deficient AM. The determination of the cellular thiol content of AM, obtained from BAL by flow cytometry, presents a simple and reliable tool to monitor the effect of therapeutic measures focusing on the stabilization of the cellular thiol status.

Aged↗
PubMed1999

[Alpha 1-protease inhibitor deficiency. Diagnosis, follow-up and therapy options].

DEFINITION: Alpha-1 antitrypsin (alpha-1 proteinase inhibitor) deficiency is characterized by a marked reduction of alpha-1 antitrypsin, the major antiprotease in man. PREVALENCE: Alpha-1 antitrypsin deficiency is one of the most common hereditary diseases in Caucasians of European descent. Alpha-1 antitrypsin deficiency is the underlying disorder in approximately 2% of all patients with chronic obstructive pulmonary disease and lung emphysema. CLINICAL MANIFESTATIONS: Young adults by the age of 30 to 45 years have a high risk for the development of lung emphysema with cough, sputum expectoration and respiratory insufficiency. There is a moderate risk of liver disease. DIAGNOSTIC PROCEDURES AND TREATMENT: The diagnosis is obtained by measurement of alpha-1 antitrypsin serum levels. Recognition of the disorder is important to prevent deterioration of the pulmonary function by early initiation of preventive measures and treatment. Therapeutic options are physiotherapy, antiobstructive medication and antibiotics. The most direct approach is the intravenous augmentation therapy with purified alpha-1 antitrypsin.

Adult↗
PubMed1999

Localization of TFF3, a new mucus-associated peptide of the human respiratory tract.

Trefoil factor family (TFF)-domain peptides (formerly P-domain peptides, trefoil factors) represent major mucin-associated peptides of the gastrointestinal tract. Here, the first localization studies on TFF3 in the lower respiratory tract of human material are presented. Immunohistochemistry revealed significant accumulation of TFF3 to mucous cells in the acini of submucosal glands and varying amounts in goblet cells at the ductular portions and the surface epithelium. TFF3 appears also as a component of the mucus, for example from patients with chronic bronchitis. Expression of TFF3 was also shown by use of the polymerase chain reaction. In contrast, TFF1 and TFF2 transcripts were hardly detectable in the human respiratory tract. Thus, a structural function of TFF3 for the airway mucus is discussed, possibly together with the mucins MUC5B and MUC5AC.

Blotting, Western↗
PubMed1999

Expression of cathepsin K in lung epithelial cells.

Alveolar and bronchial epithelial cells have been shown to have regulatory functions in the maintenance of lung structure and function. Recent evidence supports the premise that these cells can synthesize a variety of extracellular matrix components in vitro, suggesting an active participation in connective tissue remodeling. Their possible role in extracellular matrix degradation, however, is less clear. This study addresses the question of whether alveolar and bronchial epithelial cells express the highly collagenolytic and elastinolytic cysteine proteinase cathepsin K, which has recently been newly described. We provide evidence that the epithelial cell lines A549 and BEAS-2B are capable of expressing cathepsin K messenger RNA. Furthermore, we show that cathepsin K is expressed in normal bronchial epithelial cells. Western blot analyses of human lung-tissue lysates revealed specific immunoreactivity at molecular weights of 46 and 27 kD, corresponding to the procathepsin and the mature cathepsin K. Immunohistochemical analyses showed a pronounced staining of bronchial epithelial cells and in single alveolar epithelial cells. Using a specific fluorogenic cytochemical assay, the intracellular activity of the enzyme was localized. These findings demonstrate that bronchial and alveolar epithelial cells are capable of expressing cathepsin K, which could be of considerable importance for remodeling processes of the extracellular matrix in the lung.

Bronchi↗