Objective: High resolution computed tomography (HRCT) was used to assess the extent of bronchial reactivity after inhalative bronchoprovocation and dilation in hyperresponsive patients and healthy subjects.
Patients And Methods: Patients with mild intermittent asthma, 15 with a >20% decrease in FEV1 and a >10 mmHg (PC20+) in PaO2, 12 with a <20% decrease in FEV1 and a >10 mmHg (PC20-) in PaO2 after provocation, and eight healthy humans were included in the study. Changes in cross-sectional area in a total of 1256 bronchi and in bronchial wall area (792 bronchi) were evaluated after histamine-triggered bronchoprovocation and salbutamol-induced bronchodilation at high lung volumes (FVC 80%). Data were compared with the results of pulmonary function tests (FEV1, PaO2, PaCO2).
Results: In all groups, a significant decrease in bronchial cross-sectional area (P<0.001) and a significant increase in bronchial wall area (P<0.001) were observed subsequent to bronchoprovocation. After bronchodilation, the increase in cross-sectional area (P<0.001) and the further increase in airway wall area (P<0.01) were significant in all groups. In PC20+ and PC20- asthmatics, significant differences (P<0.05) in PaO2, >10 mmHg between baseline and provocation were observed. In healthy persons, the PaO2 decrease was <10 mmHg (P>0.05). After histamine provocation, the decrease in FEV1 was measured in the PC20+ group, whereas a <20% FEV1 decrease was found in the PC20- and the control groups, respectively. No significant correlations were observed between radiological data and the results of pulmonary function tests.
Conclusions: HRCT demonstrated bronchial reactivity in hyperresponsive patients and, unexpectedly, in healthy subjects. The applied pulmonary function tests failed to characterize bronchial reactions in the healthy subjects. Based on these results, HRCT is a useful tool by which to achieve a comprehensive understanding of the pathophysiological processes in asthmatic patients.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.ejrad.2004.02.005 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Arsenic-Induced Inflammatory Response via ROS-Dependent Activation of ERK/NF-kB Signaling Pathways: Protective Role of Natural Polyphenol Tannic Acid.
J Appl Toxicol
December 2024
Division of Biochemistry, ICMR-National Institute for Research in Environmental Health, Bhopal, Madhya Pradesh, India.
Arsenic (As), a highly toxic metalloid, is present throughout our environment as a result of both natural and human-related activities. Furthermore, As exposure could lead to a persistent inflammatory response, which may facilitate the pathogenesis of several diseases in various organs. This study was performed to investigate the As-induced inflammatory response and the underlying molecular mechanisms in vitro.
View Article and Find Full Text PDFFactor VIIa - antithrombin complexes are increased in asthma: relation to the exacerbation-prone asthma phenotype.
Thromb Haemost
January 2025
Department of Medicine, Jagiellonian University School of Medicine, Cracow, Poland.
Background: Asthma is associated with a prothrombotic state. Plasma factor VIIa-antithrombin complex concentrations (FVIIa-AT) indirectly reflect the interaction of tissue factor (TF) with FVII. Since TF is a key initiator of coagulation in vivo, we hypothesized that FVIIa-AT are higher in asthma.
View Article and Find Full Text PDFArtemisinin protected human bronchial epithelial cells from amiodarone-induced oxidative damage via 5'-AMP-activated protein kinase (AMPK) activation.
Redox Rep
December 2025
Pharmaceutical Science, Faculty of Health Sciences, University of Macau, Taipa, People's Republic of China.
Background: Amiodarone, a common antiarrhythmic drug, is known for its severe side effects, including pulmonary toxicity, which involves oxidative stress and apoptosis. Artemisinin, an antimalarial drug, has shown cytoprotective properties by inhibiting oxidative stress and apoptosis. This study investigated the protective effects of artemisinin against amiodarone-induced toxicity in human bronchial epithelial cells (BEAS-2B) and mouse models.
View Article and Find Full Text PDFRNA mA involves in regulation of oxidative stress and apoptosis may via NF-kB pathway in cadmium-induced lung cells.
Cell Death Discov
January 2025
Institute of Preventive Medicine, School of Public Health, Dali University, No. 22, Wanhua Road, Dali, Yunnan, 671000, PR China.
Cadmium has been identified as an environmental pollutant and a carcinogen. N-methyladenosine (mA) plays a crucial role in the development of lung tumors, but the mechanisms remain incompletely clarified. In present study, our data demonstrated that prolonged treatment of 1 μmol/L CdSO for 40 passages in bronchial epithelial cells (Beas-2B cells) resulted in the development of a malignant phenotype, which manifested as boosted proliferation, migration and invasion capacity as well as apoptosis reduction.
View Article and Find Full Text PDFClinically significant hemoptysis and all-cause mortality in patients with nontuberculous mycobacterial pulmonary disease.
Respir Med
January 2025
Biomedical Research Institute, Seoul National University Hospital, Seoul, Republic of Korea; Department of Microbiology, Harvard Medical School, Boston, United States. Electronic address:
Background: Hemoptysis is one of the major symptoms in patients with nontuberculous mycobacterial pulmonary disease (NTM-PD). However, its prevalence, incidence, and impact on long-term prognosis remain uncertain. We evaluated the incidence of clinically significant hemoptysis, and determined its association with mortality in patients with NTM-PD.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!