Changes in oxygen partial pressure of brain tissue in an animal model of obstructive apnea

Abstract

BackgroundCognitive 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.MethodsTwenty-four male Sprague-Dawley rats (300-350 g) were used. Sixteen rats were anesthetized and non-invasively 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 fast-response 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.ResultsArterial 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.ConclusionsThese data suggest that the cerebral cortex is partially protected from intermittently occurring interruption of O2 supply induced by obstructive apneas mimicking OSA.

Intermittent hypoxia alters gut microbiota diversity in a mouse model of sleep apnoea

“…Assessment of the changes in PaO 2 induced by intermittent hypoxia exposure in the bowel was carried out with an oxygen sensor that was previously used to measure PaO 2 within different tissues in animal models of OSA [4,6]. As expected, the level of oxygenation in the faeces decreased as the sensor approached the anoxic core of the intestinal content.…”

“…Whereas the magnitude and pathophysiological impact of hypoxia/re-oxygenation has been investigated in different organs and tissues such as brain, liver, testes, fat or muscle [4][5][6], no attention has been paid to the potential effect of recurrent oxygen desaturations that characterise OSA on the gut microbiota. In fact, the mammalian gut is populated by a complex and dense microbial community dominated by obligate anaerobic organisms from both the Firmicutes and Bacteroidetes phyla in a dynamic environment determined by the host physiology [7].…”

Time-dependent effect of acute hypoxia on corticospinal excitability in healthy humans

“…Such changes may be able to influence neuron excitability that is sensitive not only to hypoxia but also to changes in arterial CO 2 and circulating ions such as bicar- all et al 2010) as well as personal observations (unpublished data) regarding cortex oxygenation assessed with near-infrared spectroscopy in healthy subjects inhaling a hypoxic gas mixture at rest indicated that the kinetics of cortex deoxygenation response is noticeably longer than arterial blood deoxygenation, requiring Ͼ20 -30 min to reach a steady state. Also, recent animal studies regarding brain oxygenation under hypoxemic conditions emphasize the specificity of brain tissue oxygenation response to hypoxemia, with, for instance, some cerebral reoxygenation being observed over the course of a 1-h stable periodic pattern of hypoxemia (Almendros et al 2010). Therefore, the specific pattern of cerebral tissue deoxygenation under hypoxemic conditions could contribute to a time-dependent effect of hypoxic breathing on cortex excitability.…”

Obstructive sleep apnea

“…Almendros and colleagues [27,28] have recently examined changes in oxygen partial pressure of brain tissue (PtO 2 ) in an animal model of obstructive apnea. The model is designed to apply recurrent obstructive apneas in a stable and controlled way without other comorbidities that can occur in OSA.…”