The Role of Sleep Apnea Induced Oxidative Stress in Stroke Pathogenesis and Recovery

Purpose: Obstructive sleep apnea (OSA) is a common, but under-diagnosed comorbidity among patients with a number of age-related disorders, including stroke, Alzheimer’s disease, and Parkinson’s disease. Many of the risk factors for sleep apnea, such as obesity, are modifiable and treatment of sleep apnea itself can limit its systemic effects. Because of these facts, understanding the role of OSA in more serious diseases may promote awareness and early diagnosis, thus preventing serious adverse health outcomes. Given the knowledge that sleep apnea increases oxidative stress, in order to investigate the effects of sleep apnea on the pathogenesis of and recovery from stroke, we used chronic intermittent hypoxia (CIH) as an animal model of sleep apnea in rats. Methods: 12 rats underwent behavioral testing and were then randomly assigned to chambers with either a constant normoxic environment or one that simulates the chronic intermittent hypoxia of sleep apnea. Cerebral ischemia was induced in rats by occlusion of the middle cerebral artery. After a day of recovery, cognitive impairment, oxidative stress, and the size of the ischemic lesion was measured. Results: The experiment showed that CIH increased the size of the stroke lesion in the brain. In this setting, CIH did not appear to alter circulating oxidative stress protein measures or acute stroke behaviors. Conclusion: Based on these results, sleep apnea co-morbidity can have deleterious effects on stroke outcomes.