Effects of Intermittent Hypoxia on Pulmonary Vascular and Systemic Diseases

Abstract

Obstructive sleep apnea (OSA) causes many systemic disorders via mechanisms related to sympathetic nerve activation, systemic inflammation, and oxidative stress. OSA typically shows repeated sleep apnea followed by hyperventilation, which results in intermittent hypoxia (IH). IH is associated with an increase in sympathetic activity, which is a well-known pathophysiological mechanism in hypertension and insulin resistance. In this review, we show the basic and clinical significance of IH from the viewpoint of not only systemic regulatory mechanisms focusing on pulmonary circulation, but also cellular mechanisms causing lifestyle-related diseases. First, we demonstrate how IH influences pulmonary circulation to cause pulmonary hypertension during sleep in association with sleep state-specific change in OSA. We also clarify how nocturnal IH activates circulating monocytes to accelerate the infiltration ability to vascular wall in OSA. Finally, the effects of IH on insulin secretion and insulin resistance are elucidated by using an in vitro chamber system that can mimic and manipulate IH. The obtained data implies that glucose-induced insulin secretion (GIS) in pancreatic β cells is significantly attenuated by IH, and that IH increases selenoprotein P, which is one of the hepatokines, as well as TNF-α, CCL-2, and resistin, members of adipokines, to induce insulin resistance via direct cellular mechanisms. Clinical and experimental findings concerning IH give us productive new knowledge of how lifestyle-related diseases and pulmonary hypertension develop during sleep.

miR-3574 ameliorates intermittent hypoxia-induced cardiomyocyte injury through inhibiting Axin1

“…There is increased recognition that OSA, characterized by intermittent hypoxia (IH), is deemed as a risk factor for the development of many cardiovascular diseases such as hypertension [ 4 ], myocardial ischemia [ 6 ], heart failure [ 7 ], atherosclerosis [ 17 ], and coronary artery disease [ 18 ]. The IH leads to a number of potential adverse consequences, including activation of inflammation [ 19 ], insulin resistance [ 20 ], oxidative stress [ 21 ], sympathetic activation [ 22 ], and endothelial dysfunction [ 23 ]. Thus, it contributes to OSA-associated cardiovascular pathologies.…”

Physiological Effects of Wearing N95 Respirator on Medical Staff During Prolong Work Hours in Covid-19 Departments

“…The effect of these changes during longer shifts or where additional tape is used to seal the mask further and in those workers with pre-existing cardio-respiratory disease has not been de ned. Several studies have suggested mechanistic links between chronic intermittent hypoxemia and increased production of reactive oxygen species, endothelial dysfunction, systemic in ammation, and pulmonary hypertension 13,14 , which may lead to longer-term consequences in susceptible individuals.…”

Sleep-related breathing disorders in patients with heart failure: classification, epidemiology and pathophysiology. Part I

“…У пациентов ХСН с сопутствующим гемодинамиче-ски значимым поражением коронарных артерий это может также спровоцировать острую ишемию миокарда. Наряду со снижением сократительной функции ИГ напрямую или косвенно приводит к повышению давления в легочной артерии [46]. Нарушение газового состава крови и следующий за этим эпизод пробуждения (ЭЭГ-активация) вызывают увеличение тонуса симпатического отдела вегетативной нервной системы, которое сопровождается резким повышением системного артериального давления [47] и может привести к некрозу кардиомиоцитов и формированию аритмического очага [48].…”