11 research outputs found
Changes in oxygen partial pressure of brain tissue in an animal model of obstructive apnea
Background: Cognitive impairment is one of the main consequences of obstructive sleep apnea (OSA) and is
usually attributed in part to the oxidative stress caused by intermittent hypoxia in cerebral tissues. The presence of
oxygen-reactive species in the brain tissue should be produced by the deoxygenation-reoxygenation cycles which
occur at tissue level during recurrent apneic events. However, how changes in arterial blood oxygen saturation
(SpO2) during repetitive apneas translate into oxygen partial pressure (PtO2) in brain tissue has not been studied.
The objective of this study was to assess whether brain tissue is partially protected from intermittently occurring
interruption of O2 supply during recurrent swings in arterial SpO2 in an animal model of OSA.
Methods: Twenty-four male Sprague-Dawley rats (300-350 g) were used. Sixteen rats were anesthetized and noninvasively
subjected to recurrent obstructive apneas: 60 apneas/h, 15 s each, for 1 h. A control group of 8 rats was
instrumented but not subjected to obstructive apneas. PtO2 in the cerebral cortex was measured using a fastresponse
oxygen microelectrode. SpO2 was measured by pulse oximetry. The time dependence of arterial SpO2
and brain tissue PtO2 was carried out by Friedman repeated measures ANOVA.
Results: Arterial SpO2 showed a stable periodic pattern (no significant changes in maximum [95.5 ± 0.5%; m ± SE]
and minimum values [83.9 ± 1.3%]). By contrast, brain tissue PtO2 exhibited a different pattern from that of arterial
SpO2. The minimum cerebral cortex PtO2 computed during the first apnea (29.6 ± 2.4 mmHg) was significantly
lower than baseline PtO2 (39.7 ± 2.9 mmHg; p = 0.011). In contrast to SpO2, the minimum and maximum values of
PtO2 gradually increased (p < 0.001) over the course of the 60 min studied. After 60 min, the maximum (51.9 ± 3.9
mmHg) and minimum (43.7 ± 3.8 mmHg) values of PtO2 were significantly greater relative to baseline and the first
apnea dip, respectively.
Conclusions: These data suggest that the cerebral cortex is partially protected from intermittently occurring
interruption of O2 supply induced by obstructive apneas mimicking OSA