Continuous positive airway pressure (CPAP) induces early nasal inflammation

Abstract

Study Objectives: To assess whether noninvasive application of nCPAP is a mechanical stimulus inducing early nasal inflammation. Design: Prospective controlled animal study. Setting: University laboratory. Patients or Participants: 32 male Sprague-Dawley rats (250-300 g). Interventions: The rats were anesthetized and subjected to nCPAP=10 cm H2O and sham-CPAP through a mask for 3 h and 5 h (n=8 each). Measurements and Results: After nCPAP or sham, nasal scraping was carried out to detect neutrophils, and septum and dorsal nasal concha were excised to assess gene expression of inflammatory markers by real time PCR. Percentage of neutrophils in nucleated cells in the nasal scrapings was significantly (P = 0.006) higher after 5 h of nCPAP (3.51% ± 0.73%; m ± SEM) than in the sham group (1.12% ± 0.39%). When compared with sham, the mRNA of macrophage inflammatory protein-2 (MIP-2) in nasal tissue was significantly overexpressed after both 3 h (2.28-fold ± 0.43-fold; P = 0.034) and 5 h (5.56-fold ± 1.88-fold; P = 0.002) of nCPAP=10 cm H2O. No significant changes were found in the gene expressions of tumor necrosis factor-α, nerve growth factor and tachykinin-1 receptor. Conclusions: The compression applied by nCPAP (10 cm H2O, 5 h) on the nasal wall of healthy rats is a mechanical stimulus that triggers an early inflammatory process mediated by MIP-2, resulting in neutrophil extravasation.