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Changes in oxygen partial pressure of brain tissue in an animal model of obstructive apnea Almendros López, Isaac Montserrat Canal, José Ma. Torres, Marta González, Constancio Navajas Navarro, Daniel Farré Ventura, Ramon Escorça cerebral Malalties pulmonars obstructives cròniques Models animals en la investigació Cerebral cortex Chronic obstructive pulmonary diseases Animal models in research 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. 2012-05-16T09:08:11Z 2012-05-16T09:08:11Z 2010 info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion Reproducció del document publicat a: http://dx.doi.org/10.1186/1465-9921-11-3 Respiratory Research, 2010, vol. 11, num. 3 http://dx.doi.org/10.1186/1465-9921-11-3 cc-by (c) Almendros et al., 2010 http://creativecommons.org/licenses/by/3.0/es/ info:eu-repo/semantics/openAccess BioMed Central Articles publicats en revistes (Ciències Fisiològiques)