I Vilaseca1, E Lehrer-Coriat2, M Torres3, F Aguilar4, I Almendros5, B M Martínez-Vidal6, R Farré7, J M Montserrat8. 1. Sleep Disorders Unit Hospital Clínic, Barcelona, Spain; Ciber Enfermedades Respiratorias (CIBERES), Bunyola, Spain; Faculty of Medicine, University of Barcelona, Barcelona, Spain. Electronic address: ivila@clinic.ub.es. 2. Otolaryngology Department, Hospital Esperit Sant, Santa Coloma de Gramanet, Spain. 3. Ciber Enfermedades Respiratorias (CIBERES), Bunyola, Spain. 4. Otolaryngology Department, Hospital General de Granollers, Granollers, Spain. 5. Biophysics and Bioengineering Unit, Medicine Faculty, University of Barcelona, Barcelona, Spain. 6. Otolaryngology Department, Hospital del Sagrat Cor, Barcelona, Spain. 7. Ciber Enfermedades Respiratorias (CIBERES), Bunyola, Spain; Otolaryngology Department, Hospital Esperit Sant, Santa Coloma de Gramanet, Spain; Institut d' Investigació Biomèdica August Pi i Sunyer (IDIBAPS), Barcelona, Spain. 8. Sleep Disorders Unit Hospital Clínic, Barcelona, Spain; Ciber Enfermedades Respiratorias (CIBERES), Bunyola, Spain; Faculty of Medicine, University of Barcelona, Barcelona, Spain; Biophysics and Bioengineering Unit, Medicine Faculty, University of Barcelona, Barcelona, Spain; Institut d' Investigació Biomèdica August Pi i Sunyer (IDIBAPS), Barcelona, Spain.
Abstract
BACKGROUND: Continuous positive airway pressure (CPAP) is the most commonly used treatment in obstructive sleep apnea. In a previous rat model study, we demonstrated that nasal CPAP induces early rhinitis expressed by nasal neutrophil extravasation. Here we hypothesized that nasal CPAP would worsen nasal inflammation on a previously inflamed mucosa. The objective of this study was to evaluate the early nasal CPAP effects of allergic rhinitis (AR) in a rodent model. METHODS: Twenty Sprague-Dawley rats were sensitized with intraperitoneal ovalbumin (OVA). Nasal inflammation was induced by the administration of intranasal OVA during consecutive days. The same procedure was performed in 20 control rats treated with saline solution. The allergic (AR) and non-allergic (NAR) rats were then randomized to nasal CPAP at 10 cm H2O for five hours or to sham CPAP. The degree of nasal inflammation was assessed by evaluating the percentage of neutrophils, eosinophils, basophils, and lymphocytes in the nasal mucosa. An unpaired Mann-Whitney test was used to analyze differences between groups. RESULTS: The greatest inflammation was observed in the group of AR without CPAP (1.24% ± 0.94%), followed by NAR with CPAP (0.64% ± 0.30%), AR with CPAP (0.64% ± 0.40%), and NAR without CPAP (0.21% ± 0.29%). CONCLUSIONS: Administration of nasal CPAP or allergy sensitization can produce, individually, neutrophil extravasation on the nasal mucosa of a rat model. The application of both stimuli is not responsible for increased inflammation. Therefore, this study suggests that rhinitis is not a major limitation for CPAP administration.
BACKGROUND: Continuous positive airway pressure (CPAP) is the most commonly used treatment in obstructive sleep apnea. In a previous rat model study, we demonstrated that nasal CPAP induces early rhinitis expressed by nasal neutrophil extravasation. Here we hypothesized that nasal CPAP would worsen nasal inflammation on a previously inflamed mucosa. The objective of this study was to evaluate the early nasal CPAP effects of allergic rhinitis (AR) in a rodent model. METHODS: Twenty Sprague-Dawley rats were sensitized with intraperitoneal ovalbumin (OVA). Nasal inflammation was induced by the administration of intranasal OVA during consecutive days. The same procedure was performed in 20 control rats treated with saline solution. The allergic (AR) and non-allergic (NAR) rats were then randomized to nasal CPAP at 10 cm H2O for five hours or to sham CPAP. The degree of nasal inflammation was assessed by evaluating the percentage of neutrophils, eosinophils, basophils, and lymphocytes in the nasal mucosa. An unpaired Mann-Whitney test was used to analyze differences between groups. RESULTS: The greatest inflammation was observed in the group of AR without CPAP (1.24% ± 0.94%), followed by NAR with CPAP (0.64% ± 0.30%), AR with CPAP (0.64% ± 0.40%), and NAR without CPAP (0.21% ± 0.29%). CONCLUSIONS: Administration of nasal CPAP or allergy sensitization can produce, individually, neutrophil extravasation on the nasal mucosa of a rat model. The application of both stimuli is not responsible for increased inflammation. Therefore, this study suggests that rhinitis is not a major limitation for CPAP administration.
Authors: A Cisternas; F Aguilar; J M Montserrat; M Àvila; M Torres; A Iranzo; J Berenguer; I Vilaseca Journal: Sleep Breath Date: 2017-05-10 Impact factor: 2.816