Systemic prostacyclin and thromboxane production in obstructive sleep apnea

Mejza, Filip; Kania, Aleksander; Nadziakiewicz, Paweł; Niżankowska-Jędrzejczyk, Agata; Niżankowska‐Mogilnicka, Ewa

doi:10.1016/j.advms.2015.12.001

Cited by 5 publications

(2 citation statements)

References 26 publications

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“…It is likely that airway epithelial cells are the major source of production of ROS and cyclooxygenase metabolites because the lung epithelium is a primary target for direct insult by IH. In fact, patients with OSA are known to exhibit augmented productions of cyclooxygenase metabolites in the blood (Mejza et al, 2016 ) or the airways (Goldbart et al, 2006 ).…”

Section: Discussionmentioning

confidence: 99%

Inflammatory Role of ROS-Sensitive AMP-Activated Protein Kinase in the Hypersensitivity of Lung Vagal C Fibers Induced by Intermittent Hypoxia in Rats

Yang¹,

Shen

Lai

et al. 2016

Front. Physiol.

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Obstructive sleep apnea (OSA), manifested by airway exposure to intermittent hypoxia (IH), is associated with excess reactive oxygen species (ROS) production in airways, airway inflammation, and hyperreactive airway diseases. The cause-effect relationship for these events remains unclear. We investigated the inflammatory role of ROS-sensitive AMP-activated protein kinase (AMPK) in IH-induced airway hypersensitivity mediated by lung vagal C fibers (LVCFs) in rats. Conscious rats were exposed to room air (RA) or IH with or without treatment with N-acetyl-L-cysteine (NAC, an antioxidant), Compound C (an AMPK inhibitor), ibuprofen (a cyclooxygenase inhibitor), or their vehicles. Immediately after exposure (24 h), we found that intravenous capsaicin, phenylbiguanide, or α,β-methylene-ATP evoked augmented LVCF-mediated apneic responses and LVCF afferent responses in rats subjected to IH exposure in comparison with those in RA rats. The potentiating effect of IH on LVCF responses decreased at 6 h after and vanished at 12 h after the termination of IH exposure. The potentiating effect of IH on LVCF-mediated apneic and LVCF afferent responses was significantly attenuated by treatment with NAC, compound C, or ibuprofen, but not by their vehicles. Further biochemical analysis revealed that rats exposed to IH displayed increased lung levels of lipid peroxidation (an index of oxidative stress), AMPK phosphorylation (an index of AMPK activation), and prostaglandin E2 (a cyclooxygenase metabolite), compared with those exposed to RA. IH-induced increase in lipid peroxidation was considerably suppressed by treatment with NAC but not by compound C or ibuprofen. IH-induced increase in AMPK phosphorylation was totally abolished by NAC or compound C but not by ibuprofen. IH-induced increase in prostaglandin E2 was considerably prevented by any of these three inhibitor treatments. The vehicles of these inhibitors exerted no significant effect on the three IH-induced responses. These results suggest that 24-h IH exposure sensitizes LVCFs, leading to an exaggerated reflex and afferent responses to chemical stimulants in rats. Moreover, this IH-induced LVCF sensitization is mediated through a cascade of inflammatory responses in the airways involving increases in ROS, AMPK activation, and cyclooxygenase metabolite release.

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Section: Discussionmentioning

confidence: 99%

Inflammatory Role of ROS-Sensitive AMP-Activated Protein Kinase in the Hypersensitivity of Lung Vagal C Fibers Induced by Intermittent Hypoxia in Rats

Yang¹,

Shen

Lai

et al. 2016

Front. Physiol.

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“…Overall, these findings support the potential implications of circulating MP-associated endothelial dysfunction in OSA patients. [15,16] There are evidences that OSA is associated with inflammation of the blood vessels, which is considered to be a major cause of the atherogenic process. OSA patients have increased serum levels of TNF-a, IL-6, IL-8, CRP and adhesion molecules (CD62L, soluble CD62E, CD62P, Intercellular Adhesion Molecule-1 (ICAM-1) and Vascular Adhesion Molecule-1 (VCAM-1).…”

Section: The Role Of Microparticles In Osa Patientsmentioning

confidence: 99%

The Role of Cyclooxygenase Enzymes and Microparticles in Obstructive Sleep Apnea Related Cerebrovascular Incidents

Togatorop

Utami

2023

Int J Res Rev

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Obstructive Sleep Apnea (OSA) is a sleep disorder caused by breathing problems that occur during sleep due to airway obstruction. Obstructive Sleep Apnea is quite common, but is often overlooked and misdiagnosed and untreated. Many studies have proven the relationship between OSA and pathological diseases such as cardiovascular disease and stroke. Intermittent Hypoxia (IH) that occurs in OSA patients can cause endothelial dysfunction and play a role in the atherogenesis of peripheral and central blood vessels of the brain. Hypoxic conditions cause the release of microparticles, inflammatory mediators and increase the expression of the enzyme Cyclooxygenase (COX) in the vascular endothelium. This causes an increase in inflammation-related prostanoid production which in turn causes endothelial damage and increases the risk of atherosclerotic plaque formation. This review article will discuss the role of inflammatory mediators, especially COX enzymes in OSA-related cerebrovascular incidents. Keywords: cerebrovascular incidents, cyclooxygenase, intermittent hypoxia, obstructive sleep apnea

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Overnight Change in Urinary Prostacyclin and Thromboxane in Obstructive Sleep Apnea

Suárez-Girón

Almendros

Roca‐Ferrer

et al. 2019

Archivos de Bronconeumología (English Edition)

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Systemic prostacyclin and thromboxane production in obstructive sleep apnea

Cited by 5 publications

References 26 publications

Inflammatory Role of ROS-Sensitive AMP-Activated Protein Kinase in the Hypersensitivity of Lung Vagal C Fibers Induced by Intermittent Hypoxia in Rats

Inflammatory Role of ROS-Sensitive AMP-Activated Protein Kinase in the Hypersensitivity of Lung Vagal C Fibers Induced by Intermittent Hypoxia in Rats

The Role of Cyclooxygenase Enzymes and Microparticles in Obstructive Sleep Apnea Related Cerebrovascular Incidents

Overnight Change in Urinary Prostacyclin and Thromboxane in Obstructive Sleep Apnea

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