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

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 (15s each, 60/h, for 3h); (3) apnea+O(2): 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-kappaB in the lung and diaphragm.

RESULTS

TNF-alpha and IL-1beta significantly increased in all groups compared with sham. NF-kappaB in the lung was increased in apnea and hypoxia/normoxia groups, but not in apnea+O(2) group. In diaphragm tissue, NF-kappaB was only significant in apnea compared to sham. Significant differences were found in the ratio thromboxane-B2/6-keto-Prostaglandin-F1alpha between apnea and hypoxia/normoxia compared to sham but not in apnea+O(2).

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.