Obstructive sleep apnea is a newly recognized significant risk factor for hypertension, myocardial infarction, stroke and cognitive dysfunction; this disorder disturbs metabolic function, promoting insulin resistance and impairing metabolism. Characterized by frequent episodes of upper airway obstruction resulting in hypoxia and sleep disruption, obstructive sleep apnea is present in over 2% of the population in developed countries. Using diverse models of sleep apnea, in animals and humans, researchers have made significant progress in understanding the mechanisms underlying cardiovascular, neurologic and endocrinologic morbidities of obstructive sleep apnea, while pharmacologic therapies for obstructive sleep apnea remain elusive. In this issue of Frontiers in Neurology, we propose to highlight the clinically relevant questions that must be answered to successfully treat obstructive sleep apnea and its co-morbidities. We will then describe the progress made and future promise with the various models of obstructive sleep apnea. With effective well-orchestrated use of the highly complementary models, we may most effectively expedite therapies for this common disorder, one that is associated with so much morbidity.
Moderate to severe obstructive sleep apnea (OSA) occurs in 10-17% of middle aged men and 3-9% of middle-aged women with a higher prevalence among obese subjects. This condition is an independent risk factor for many cardiovascular diseases. Intermittent hypoxia is a major pathophysiologic character of OSA; it can lead to oxidative stress and inflammation, which in their turn cause endothelial dysfunction, a hallmark of atherosclerosis. Many animal models have been designed to mimic OSA in human patients to allow more in-depth investigation of biological and cellular mechanisms of this condition. This review discusses the cardiovascular outcomes of OSA and some of the animal models that are being used to investigate it.