Brief CommunicationEarly effects of continuous positive airway pressure in a rodent model of allergic rhinitis
Introduction
Obstructive sleep apnea syndrome (OSAS) is a prevalent disorder characterized by recurrent partial or total upper airway closure during sleep. The most widespread treatment for OSAS is the nocturnal application of continuous positive airway pressure (CPAP) through the nose. However, only 50–80% of patients initially accept nasal CPAP, and sufficient long-term compliance varies between 17% and 71% [1].
Some of the reasons that patients experience CPAP intolerance are nasal secondary effects. The mechanism could be due to a compression stimulus during the application of CPAP. Positive pressure triggers a biological response in a variety of cells in the nose as well as in the airways [2], [3], [4] and may cause nasal symptoms. It has also been suggested that pre-existing nasal obstruction or previous symptoms of nasal inflammation could be exacerbated by CPAP and therefore increase symptoms and contribute to poor patient compliance [5].
In a previous study, we demonstrated that nasal CPAP induces early local inflammation resulting in neutrophil extravasation in the nasal mucosa of healthy rats [6]. However, the impact of nasal CPAP on a previously inflamed mucosa has not yet been fully assessed. Our hypothesis was the following: When a previous nasal inflammation exists, a second source of injury (ie, CPAP) would worsen the nasal inflammation.
Therefore, the aim of our study was to evaluate early CPAP effects in a rat model of allergic rhinitis (AR).
Section snippets
Methods
The study was approved by the Ethics Committee for Animal Experimentation of the University of Barcelona. Twenty Sprague-Dawley rats were sensitized with intraperitoneal ovalbumin (OVA). Nasal inflammation was induced by the administration of OVA intranasal drops during 24 consecutive days (Fig. 1). The same procedure was performed in 20 control rats treated with saline solution. The allergic (AR) and non-allergic (NAR) rats were then anesthetized (urethane, 1 g/kg) and randomized to 5 h of
Results
Nasal cytology showed that the cells most commonly detected in the nasal mucosa were neutrophils, which define a condition of minimal inflammation. The highest neutrophil extravasation rate was observed in the group with allergic rhinitis without CPAP (AR/Sham-CPAP), followed by non-allergic rhinitis with CPAP (NAR/CPAP), allergic rhinitis with CPAP (AR/CPAP), and non-allergic rhinitis without CPAP (NAR/Sham-CPAP) (Fig. 2). There were significant differences between AR/Sham-CPAP and
Discussion
The results obtained in the present study confirmed our previous findings that the application of CPAP in the nasal mucosa in a rat model induces neutrophil extravasation [6], [7]. Moreover, the induction of rhinitis by means of intraperitoneal nasal sensitization to OVA was also responsible for a significant increase in neutrophil extravasation in the nasal mucosa of the animals, whereas no significant eosinophil, basophil, or lymphocyte-related inflammation could be found. Contrary to initial
Funding
This work was supported in part by FIS PI07/0318, co-financed by FEDER and CIBERES.
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