RT Journal Article SR Electronic T1 Carotid body inflammation and cardiorespiratory alterations in intermittent hypoxia JF European Respiratory Journal JO Eur Respir J FD European Respiratory Society SP 1492 OP 1500 DO 10.1183/09031936.00141511 VO 39 IS 6 A1 Rodrigo Del Rio A1 Esteban A. Moya A1 María J. Parga A1 Carlos Madrid A1 Rodrigo Iturriaga YR 2012 UL http://erj.ersjournals.com/content/39/6/1492.abstract AB Chronic intermittent hypoxia (CIH), a main feature of obstructive sleep apnoea (OSA), increases hypoxic ventilatory responses and elicits hypertension, partially attributed to an enhance carotid body (CB) responsiveness to hypoxia. As inflammation has been involved in CIH-induced hypertension and chemosensory potentiation, we tested whether ibuprofen may block CB chemosensory and cardiorespiratory alterations induced by CIH in a rat model of OSA. We studied the effects of ibuprofen (40 mg·kg−1·day−1) on immunohistochemical interleukin (IL)-1β and tumour necrosis factor (TNF)-α levels in the CB, the number of c-fos-positive neurons in the nucleus tractus solitarii (NTS), CB chemosensory and ventilatory responses to hypoxia, and arterial blood pressure in male rats either exposed for 21 days to 5% O2 (12 episodes·h−1, 8 h·day−1) or kept under sham condition. CIH increased CB TNF-α and IL-1β and c-fos-positive neurons in the NTS, enhanced carotid chemosensory and ventilatory hypoxic responses, and produced hypertension. Ibuprofen prevented CB cytokine overexpression and CIH-induced increases in c-fos-positive neurons in the NTS, the enhanced hypoxic ventilatory responses and hypertension, but failed to impede the CB chemosensory potentiation. Results suggest that pro-inflammatory cytokines may contribute to the CIH-induced cardiorespiratory alterations, acting at several levels of the hypoxic chemoreflex and cardiovascular control pathways.