Biological consequences of oxygen desaturation and respiratory effort in an acute animal model of obstructive sleep apnea (OSA)

Abstract Background An animal model mimicking all the factors involved in obstructive sleep apnea (OSA) is useful for investigating mechanisms because the associated comorbidity usually present in such patients is an important limitation. Aim To test the hypothesis that hypoxia/normoxia and respiratory effort have different effects on the induction of inflammatory response and endothelial dysfunction in an acute rat model of OSA. Methods Four groups of anesthetized rats were studied ( n = 8): (1) sham; (2) apnea: obstructions (15 s each, 60/h, for 3 h); (3) apnea + O2 : obstructions and breathing oxygen-enriched air to avoid hypoxia and (4) intermittent hypoxia/normoxia. Inflammatory and endothelial mediators were measured as outcomes along with NF-κB in the lung and diaphragm. Results TNF-α and IL-1β significantly increased in all groups compared with sham. NF-κB in the lung was increased in apnea and hypoxia/normoxia groups, but not in apnea + O2 group. In diaphragm tissue, NF-κB was only significant in apnea compared to sham. Significant differences were found in the ratio thromboxane-B2/6-keto-Prostaglandin-F1α between apnea and hypoxia/normoxia compared to sham but not in apnea + O2. Conclusions Oxygen desaturations and respiratory efforts play a role in the induction of systemic inflammation but only hypoxia/normoxia induces endothelial dysfunction. These data suggest a potential role for oxygen therapy in patients with OSA.