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Is intermittent hypoxia good or bad? Endothelial function plays a central role.

Editorial: Intermittent Hypoxia: From Basic Mechanisms to Clinical Insights and Therapeutics Lena Lavie
The implications of various forms of hypoxia to physiological or pathological conditions are enormous. In this manuscripts’ collection of “Research Topics,” expert authors focused on the effects of intermittent hypoxia (IH), the hallmark of obstructive sleep apnea (OSA) on physiological and pathophysiological conditions and potential treatments, each, contributing original research articles and reviews in their field.
REVIEW Novel Mechanisms of Myocardial Ischemia, Ischemia-Reperfusion, and Protection by Myocardial Conditioning Cardioprotection by intermittent hypoxia conditioning: evidence, mechanisms, and therapeutic potential
Robert T. Mallet,1 Eugenia B. Manukhina,1,2,3 Steven Shea Ruelas,1 James L. Caffrey,1 and H. Fred Downey1,3 1
Department of Integrative Physiology and Anatomy, University of North Texas Health Science Center, Fort Worth, Texas; 2 Institute of General Pathology and Pathophysiology, Russian Academy of Medical Sciences, Moscow, Russian Federation; and 3 School of Medical Biology South Ural State University, Chelyabinsk, Russian Federation
Am J Physiol Heart Circ Physiol 315: H216 –H232,
The calibrated application of limited-duration, cyclic, moderately intense hypoxia-reoxygenation increases cardiac resistance to ischemia-reperfusion stress. These intermittent hypoxic conditioning (IHC) programs consistently produce striking reductions in myocardial infarction and ventricular tachyarrhythmias after coronary artery occlusion and reperfusion and, in many cases, improve contractile function and coronary blood flow. These IHC protocols are fundamentally different from those used to simulate sleep apnea, a recognized cardiovascular risk factor. In clinical studies, IHC improved exercise capacity and decreased arrhythmias in patients with coronary artery or pulmonary disease and produced robust, persistent, antihypertensive effects in patients with essential hypertension. The protection afforded by IHC develops gradually and depends on -adrenergic, -opioidergic, and reactive oxygen-nitrogen signaling pathways that use protein kinases and adaptive transcription factors. In summary, adaptation to intermittent hypoxia offers a practical, largely unrecognized means of protecting myocardium from impending ischemia. The myocardial and perhaps broader systemic protection provided by IHC clearly merits further evaluation as a discrete intervention and as a potential complement to conventional pharmaceutical and surgical interventions.
KEYWORDS: enkephalin; glycolysis; mitochondrial permeability transition; myocardial ischemia; nitric oxide; protein kinase; reactive oxygen species; sarcoplasmic reticulum