Obturacyjny bezdech senny a śródbłonek naczyniowy. Czy dysponujemy komórkowymi markerami dysfunkcji śródbłonka?

*Małgorzata Dec, Elżbieta Bartoszek, Jerzy Mosiewicz

Summary
Obstructive sleep apnea (OSA) is known to be an independent risk factor of cardiovascular disease and endothelial dysfunction. Episodes of hypoxemia in OSA occur repeatedly during the night and can lead to hypertension, atherosclerosis, diabetes mellitus, coronary disease, congestive cardiac failure, stroke and cardiac arrhythmias. The sources of endothelial dysfunction in OSA are still not clear but, are probably linked with intermittent repeating episodes of hypoxemia, which induce oxidative stress, reactive oxygen species production and increase the activity of proinflammatory factors. It results in the alterations of endothelial hormones, leads to vasoconstriction, vascular smooth muscle proliferation and increase hypercoagulability. Endothelial dysfunction results in precipitating atherosclerosis. Endothelial microparticles, circulating endothelial cells and circulating endothelial progenitors cells are the cellular biomarkers of vascular damage. They have direct insight into the state of endothelium and the mechanism of vascular dysfunction. It is crucial to undertake futher research into cellular biomarkers based on the properly selected patients and the standardized methods of detection of this cells.

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