Tissue Oxygenation in Brain, Muscle, and Fat in a Rat Model of Sleep Apnea: Differential Effect of Obstructive Apneas and Intermittent Hypoxia

Abstract

To test the hypotheses that the dynamic changes in brain oxygen partial pressure (PtO₂) in response to obstructive apneas or to intermittent hypoxia differ from those in other organs and that the changes in brain PtO₂ in response to obstructive apneas is a source of oxidative stress. Prospective controlled animal study. University laboratory. 98 Sprague-Dawley rats. Cerebral cortex, skeletal muscle, or visceral fat tissues were exposed in anesthetized animals subjected to either obstructive apneas or intermittent hypoxia (apneic and hypoxic events of 15 s each and 60 events/h) for 1 h. Arterial oxygen saturation (SpO₂) presented a stable pattern, with similar desaturations during both stimuli. The PtO₂ was measured by a microelectrode. During obstructive apneas, a fast increase in cerebral PtO₂ was observed (38.2 ± 3.4 vs. 54.8 ± 5.9 mm Hg) but not in the rest of tissues. This particular cerebral response was not found during intermittent hypoxia. The cerebral content of reduced glutathione was decreased after obstructive apneas (46.2% ± 15.2%) compared to controls (100.0% ± 14.7%), but not after intermittent hypoxia. This antioxidant consumption after obstructive apneas was accompanied by increased cerebral lipid peroxidation under this condition. No changes were observed for these markers in the other tissues. These results suggest that cerebral cortex could be protected in some way from hypoxic periods caused by obstructive apneas. The increased cerebral PtO₂ during obstructive apneas may, however, cause harmful effects (oxidative stress). The obstructive apnea model appears to be more adequate than the intermittent hypoxia model for studying brain changes associated with OSA.