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.