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

Abstract

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 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.

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.

Figure 1

Time course of the values of arterial oxygen saturation (SpO₂) and brain tissue O₂ partial pressure (PtO₂) recorded in control rats. No changes were found in SpO₂ and PtO₂ values over the 60 min of the experiment. Results are shown as mean ± SE (n = 8). The time dependence of arterial SpO₂ and brain tissue PtO₂ was assessed with a Friedman repeated measures ANOVA by comparing sample points at the first apnea and during the apneas at minute 10 and every 10 min up to 1 h with respect to baseline.

Figure 2

Example of oxygen arterial saturation (SpO₂) and brain tissue O₂ partial pressure (PtO₂) signals recorded during the first ten minutes from a rat subjected to recurrent obstructive apneas. The SpO₂ dips, mimicking those observed in OSA patients, were paralleled by similar dips in PtO₂. However, while maximum and minimum values in SpO₂ showed a stable pattern (top), PtO₂ exhibited a progressive tendency to increase (bottom).

Figure 3

Time course of the maximum (Δ) and minimum (▼) values of arterial oxygen saturation (SpO₂) and brain tissue O₂ partial pressure (PtO₂) recorded during each obstructive apnea. A schematic representation of the corresponding dips in both variables is superimposed for the purpose of clarity. Baseline value is represented by an open circle. Maximum and minimum values of PtO₂ experienced a time-dependent increase (both, p < 0.001). In contrast, no changes were found in SpO₂ maximum and minimum values. Results are shown as mean ± SE (n = 16). The time dependence of arterial SpO₂ and brain tissue PtO₂ was assessed with Friedman repeated measures ANOVA by comparing sample points at the first apnea and during the apneas at minute 10 and every 10 min up to 1 h with respect to baseline for maximum values or first event for minimum values. Comparisons were undertaken by means of the Student-Newman-Keuls method. * p < 0.05 respect to baseline ✟ p < 0.05 respect to the first apneic event.