Obstructive sleep apnoea syndrome (OSAS) is characterized by recurrent episodes of airways obstruction during sleep causing concurrent episodes of hypoxia and restoration of normal blood PO₂. The high incidence and the cardiovascular pathologies associated make of OSAS a clinical entity of great socio-economical impact. The mechanisms of genesis of the recurrent airways obstruction as well as the pathogenesis of cardiovascular processes associated to OSAS are poorly understood. A nowadays popular hypothesis is that the hypoxic-reoxygenation episodes mimic at some extent ischemia-reperfusion episodes, and therefore that a peaks of reactive oxygen species (ROS) are generated with each apnoeic episode. Animal models of SAOS consist of repeated cycles of intermittent hypoxia. Severity and the frequency of hypoxic cycles can be selected by the experimenter.

We have used adult Wistar male rats subjected to intermittent hypoxia 30 cycles/hour, with nadir PO₂ in the chambers of 72 (10% O₂) and 36 (5% O₂) mmHg, eight h/day, 15 days. On day 16^th, rats were anaesthetized and tissues were removed for analyses. We have measured GSH and GSSG, LPO and aconitase and fumarase activities in liver, brain and lung as markers of oxidative stress. We have also determined glutathione peroxidase (GPx), catalase and superoxide dismutases (SODs) as indexes of ROS disposal capacity. There were minor tissue-specific changes in all measured parameters that we consider unlikely to generate cardiovascular pathologies.

Grants: BFU2007-61848 (DGICYT), CIBER CB06/06/0050 (FISS-ICiii) and JCyL-GR242.