Active clinical trials for "Pulmonary Disease, Chronic Obstructive"

In animal models, sodium pyruvate has been shown to be an effective anti-inflammatory agent, and in human studies sodium pyruvate has been shown to be a bronchodilating agent. Subjects with COPD are known to have inflammation in the lung, and often have bronchoconstriction. As such, these subjects typically are on multiple therapies, including steroid therapy. This trial will study the effect of inhaled sodium pyruvate on inflammation and lung function in COPD subjects over a six week period.

This randomized, double-blind, placebo-controlled trial assessed the efficacy of montelukast in the treatment of adults ≥50 years of age with persistent asthma and/or COPD. Primary outcomes included forced expiratory volume in one-second (FEV1) and daytime asthma symptoms scores. Nocturnal symptoms, asthma control, health-related quality of life, peak flow measurements, and health care utilization were also assessed as secondary outcomes. Participants were recruited from the Kaiser Permanente Northwest member population. One hundred forty-nine subjects were randomized to treatment with montelukast (10 mg per day) or placebo, and were followed for a six-week period. No differences in lung function measures, health-related quality of life, health care utilization, and asthma symptom scores were observed; however, the montelukast group had slightly improved asthma control scores compared to the placebo group.

Human and animal studies have shown that inhaled corticosteroids (ICS) decrease airway blood flow . This effect is immediate (within 30 minutes), transient (lasting 90 minutes), and in animal studies independent of gene expression. In COPD patients, decrease in bronchial blood flow may also decrease mucosal edema, airway resistance and improve small airway function. If such an effect exists, then we should be able to measure improvements in airway conductance and reduce lung hyperinflation, which would have salutary effects on dyspnea and exercise endurance. To our knowledge, no study has examined the immediate effect of ICS on small airway function in COPD. The purpose of this study is to examine the effects of nebulized Pulmicort on small airway function (spirometry, plethysmographic lung volumes, airways resistance, closing volume, partial flow-volume loop analysis) and exercise endurance in patients with moderate to severe COPD. HYPOTHESIS Nebulized ICS will immediately improve airway function compared with placebo (nebulized saline). Enhanced lung emptying and reduced operating lung volumes during rest and exercise following ICS therapy will translate acutely into clinically important reductions in exertional dyspnea and improvements in exercise endurance.

The study will evaluate bioequivalence, pharmacokinetics, safety, and tolerability of Budesonide, Glycopyrronium and Formoterol (BGF) metered dose inhaler (MDI) formulated with hydrofluoroolefin (HFO) [Test] and hydrofluoroalkane (HFA) [Reference] in healthy participants (male or female).

Background: Patients with COPD often experience skeletal muscle dysfunction. For those who are unable or unwilling to undertake physical training, neuromuscular electrical stimulation (NMES) may provide an alternative method of exercise training. Objective: To investigate the effects of adding neuromuscular electrical stimulation of gluteus maximus, quadriceps and calf muscles to chest physiotherapy, compared to chest physiotherapy alone, on muscles strength (gluteus max., quadriceps, calf muscles and anterior tibial group), femoral blood flow physical and pulmonary function in severe COPD Patients.

To investigate the effects of resistant proprioceptive neuromuscular facilitation exercises on physical fitness, respiratory muscle strength, walking distance and quality of life in chronic obstructive pulmonary patients.

This is a phase 1, open-label, parallel cohort study to evaluate the PK, safety and tolerability of nebulized ensifentrine following administration of single and multiple doses in healthy Chinese male subjects.

Chronic Obstructive Pulmonary Disease (COPD) causes obstruction to airflow when breathing out. It is a leading cause of chronic lung disease, hospitalization and death. Smoking is the major cause of COPD but why some smokers develop COPD while others do not is poorly understood. A central feature of COPD is accumulation of inflammatory blood cells, macrophages and neutrophils, in the airway, leading to lung injury and airway damage. The small airways of many patients with COPD contain bacteria, which are absent in healthy smokers or non-smokers. These bacteria stimulate recruitment of neutrophils, macrophages and other inflammatory cells, further accelerating airway injury. The investigators and others have shown resident macrophages in the lung and inflammatory cells (neutrophils and macrophages) recruited from the blood, which normally clear bacteria, have reduced anti-bacterial capacity in COPD and that their altered function impairs the resolution of inflammation. The investigators now wish to test why these cells fail to clear bacteria focusing in particular on how they use molecules as food to generate energy, a process termed metabolism, since this is an important determinant of immune cell function. Comparison will be made between lung resident cells (obtained by performing bronchoscopy and washing a segment of lung to flush out immune cells) and those from the blood to determine if the alterations are specific to the lung. The investigators will identify alterations in responses to bacteria in relation to changes in metabolism . A major focus will be on how structures in the cell that normally are key for energy production (i.e. mitochondria) become dysfunctional and how this impacts responses to bacteria. The investigators will relate findings to the clinical features of COPD and to healthy non-smokers and smokers to separate smoking-related changes from COPD. The aim is to develop new approaches with which to treat and manage COPD.

The goal of this clinical trial is to learn about the therapeutic effect of Chinese traditional exercise Tai Chi in elderly acute exacerbation of chronic obstructive pulmonary disease (AECOPD) with malnutrition. The main questions it aims to answer are: Improvement of pulmonary function in patients with Tai Chi exercise; Improvement of pulmonary function in patients with Tai Chi exercise. The patients in control group were given routine nursing care model, including: Providing basic nursing care and protection for patients according to their needs, paying attention to the care of patients' airways, and providing relevant protection and auxiliary interventions according to the needs of patients when carrying out nebulized inhalation interventions; Customized nutritional supplementation recipes by specialists in clinical nutrition, giving high-protein and low-carbohydrate diets, and giving enteral or parenteral nutritional support to those who have insufficient food intake through the mouth; Carrying out health education and psychological care to alleviate the patients' psychological burdens. On the basis of the routine care model of the control group, a Tai Chi training program was developed in Tai Chi group. Tai Chi training lasted for a total of 6 months, with 4 training sessions scheduled per week, each session lasting about 40 minutes. Experts from Anqing Tai Chi Association were invited to guide the training. The training program consists of a 5-minute pre-training warm-up, a 30-minute Tai Chi exercise, and a 5-minute post-training stretching session. The Tai Chi training was done at a moderate intensity, with the heart rate limited to 60%~80% of the maximal heart rate, where: maximal heart rate=220-age. Accelerometers were worn for each member to record heart rate changes during training, and when the heart rate exceeded the standard range, the exercise intensity could be adjusted to keep the heart rate within a reasonable range.

Mild to moderate pulmonary hypertension is a common complication of chronic obstructive pulmonary disease (COPD); such a complication is associated with increased risks of exacerbation and decreased survival. A small proportion of COPD patients may present with severe pulmonary hypertension, defined by a mean pulmonary artery pressure more than 35 mmHg (or more than 20 mmHg with a low cardiac index < 2 l/min/m2) with pulmonary vascular resistance more than 3 Wood units, measured by right heart catheterization (RHC). In these patients, pulmonary microvessels remodeling is the main cause of increase in pulmonary arterial pressure and is thought to result from the combined effects of hypoxia, inflammation, and loss of capillaries but the mechanisms are complex. For these patients, no drugs have been approved for treatment and lung transplantation must be considered for the more severe patients who are eligible. A better characterization of these patients is needed. We hypothesize that microvesicles generation and endothelial damage could be related to the severity of pulmonary hypertension due to COPD, assessed by pulmonary hemodynamic parameters. Circulating biomarkers of vascular damage and cell activation will be measured in blood samples from 80 COPD patients who have hemodynamic assessment by RHC. To go further, the origin of the particles will be characterized.