Anti‐inflammatory treatment did not prevent the enhanced rat carotid chemosensory responses to acute hypoxia induced by intermittent hypoxia

Chronic intermittent hypoxia (CIH), a main feature of obstructive sleep apnea, enhances carotid body (CB) chemosensory responses to acute hypoxia. The CIH‐induced chemosensory potentiation has been attributed to increased levels of reactive oxygen species (ROS) in the CB, but it is matter of debate if ROS perse may increase CB discharges. We found that CIH‐induced a ROS‐dependent increases of TNF‐α and IL‐1β within the CB, suggesting that these pro‐inflammatory cytokines may mediate the ROS‐induced potentiation. Thus, we studied the effect of ibuprofen (IB) on the CB chemosensory potentiation and the increased TNF‐α and IL‐1β levels induced by CIH. Male Sprague‐Dawley rats implanted with subcutaneous osmotic pumps filled with IB (60 mg/kg) were exposed for 21 days to 5%O 2 , 12 times/hr for 8 hr. Using immunohistochemistry, we measured the TNF‐α and IL‐1β relative expression in the CB. The carotid chemosensory discharge was recorded from anesthetized rats in response to several levels of inspired O 2 (5–100%). We found that IB reduced the increased CB levels of TNF‐α and IL‐1β induced by CIH. In addition, IB reduced the enhanced CB basal discharge, but did not prevent the potentiated chemosensory responses to acute hypoxia induced by CIH. Thus, our results suggest that IL‐1β and TNF‐α did not contribute to enhance the CB chemosensory responses to hypoxia induced by CIH. Supported by FONDECYT 1100405