Early decrease of oxidative stress by non-invasive ventilation in patients with acute respiratory failure

Abstract

Oxidative stress plays an important role in chronic respiratory diseases where the use of non-invasive ventilation seems to reduce the oxidative damage. Data on acute respiratory failure are still lacking. The aim of the study is to investigate the interplay between oxidative stress and acute respiratory failure, and the role of non-invasive ventilation in this setting. We enrolled 60 patients suffering from acute respiratory failure (PaO/FiO ratio <300): 30 consecutive patients treated with non-invasive ventilation and 30 consecutive patients treated with conventional oxygen therapy. Serum levels of soluble Nox2-derived peptide (sNOX2-dp), a marker of NADPH-oxidase activation, and 8-iso-PGF2α and HO, markers of oxidative stress, were evaluated at baseline and after 3 h of treatment. At baseline, higher values of sNOX2-dp, 8-iso-PGF2α and HO are associated with lower values of PaO/FiO ratio (p < 0.001). After 3 h, serum levels of sNOX2-dp, HO, and 8-iso-PGF2α significantly decrease in patients treated with non-invasive ventilation, but not in patients treated with conventional oxygen therapy. Delta changes of oxidative stress parameters correlate inversely with the delta changes of PaO/FiO (R = -0.623, p < 0.001 for sNOX2-dp; R = -0.428, p < 0.001 for HO; R = -0.548, p < 0.001 for 8-iso-PGF2α). In the acute respiratory failure setting, treatment with non-invasive ventilation reduces the levels of oxidative stress in the first hours. This reduction is associated with an improvement of PaO/FiO ratio as well as in a reduction of NADPH-oxidase activity.

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“…The term oxidative stress describes the unbalance between production of reactive oxygen species (ROS) and antioxidant clearance (Sies, 2015). Unfavorable conditions, such as obesity, diabetes, hypertension or dyslipidemia, have been recognized as causes of increased ROS levels (Violi et al, 2017b; Garramone et al, 2018). Evidences supported the strong relationship between oxidative stress and CVD, including atherosclerosis (Steinberg et al, 1989; Steinberg, 2009; Steinberg and Witztum, 2010).…”

Oxidative stress and cardiovascular disease: new insights

“…In physiological conditions, ROS concentrations fluctuate in a controlled manner and are modulated by enzymatic and non-enzymatic antioxidant systems [2]. If this homeostatic state fails, such as in the case of hypertension, dyslipidaemia, diabetes, and obesity and acute conditions such as sepsis and respiratory failure, ROS levels increase [3,4]. Also, xenobiotic triggers can influence the antioxidant status, among them: radiation, drugs, habits like smoking, and environmental agents.…”

Alterations in Serum Adropin, Adiponectin, and Proinflammatory Cytokine Levels in OSAS

“…On the other hand, the intermittent hypoxemia related desaturation and reoxygenation pattern activates the oxidative stress system, thereby resulting in the formation of reactive oxygen products. is disrupts the synthesis and synthesisdegradation balance of oxidant-antioxidant metabolites [12]. Proofs acquired as a result of studies carried out during the last two decades support the necessity of considering OSAS-related sleep disorder as a low level of chronic inflammatory disease.…”

“…Proofs acquired as a result of studies carried out during the last two decades support the necessity of considering OSAS-related sleep disorder as a low level of chronic inflammatory disease. Accordingly, it is considered that a portion of the morbid phenotypic development in OSAS can be explained causally by the underlying inflammatory processes that induce end-organ function disorder [11,12].…”