Hypercapnic acidosis confers antioxidant and anti-apoptosis effects against ventilator-induced lung injury

Yang, Wanchao; Song, Chun-yu; Wang, Nan; Zhang, Lili; Yue, Ziyong; Cui, Xiaoqian; Zhou, Huacheng

doi:10.1038/labinvest.2013.118

Cited by 10 publications

(9 citation statements)

References 46 publications

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“…Notably, the addition of the nitric oxide synthase inhibitor L-NMMA had no significant effect on rhodamine production in either normocapnia or hypercapnia, indicating that the antioxidant effects of hypercapnic acidosis observed in this study were independent of peroxynitrite production and thus likely resulted from a decrease in O À 2 and/or H 2 O 2 [52]. Yang et al [53] further explored the protective, antioxidant effect of hypercapnic acidosis in 2013. Similar to Nichol et al [52] this study examined the effects of hypercapnic acidosis in lung injury during mechanical ventilation using multiple histological markers of lung damage.…”

Section: Reactive Oxygen Species/metabolismmentioning

confidence: 72%

Carbon dioxide-dependent signal transduction in mammalian systems

et al. 2021

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Carbon dioxide (CO 2 ) is a fundamental physiological gas known to profoundly influence the behaviour and health of millions of species within the plant and animal kingdoms in particular. A recent Royal Society meeting on the topic of ‘Carbon dioxide detection in biological systems' was extremely revealing in terms of the multitude of roles that different levels of CO 2 play in influencing plants and animals alike. While outstanding research has been performed by leading researchers in the area of plant biology, neuronal sensing, cell signalling, gas transport, inflammation, lung function and clinical medicine, there is still much to be learned about CO 2 -dependent sensing and signalling. Notably, while several key signal transduction pathways and nodes of activity have been identified in plants and animals respectively, the precise wiring and sensitivity of these pathways to CO 2 remains to be fully elucidated. In this article, we will give an overview of the literature relating to CO 2 -dependent signal transduction in mammalian systems. We will highlight the main signal transduction hubs through which CO 2 -dependent signalling is elicited with a view to better understanding the complex physiological response to CO 2 in mammalian systems. The main topics of discussion in this article relate to how changes in CO 2 influence cellular function through modulation of signal transduction networks influenced by pH, mitochondrial function, adenylate cyclase, calcium, transcriptional regulators, the adenosine monophosphate-activated protein kinase pathway and direct CO 2 -dependent protein modifications. While each of these topics will be discussed independently, there is evidence of significant cross-talk between these signal transduction pathways as they respond to changes in CO 2 . In considering these core hubs of CO 2 -dependent signal transduction, we hope to delineate common elements and identify areas in which future research could be best directed.

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Section: Reactive Oxygen Species/metabolismmentioning

confidence: 72%

Carbon dioxide-dependent signal transduction in mammalian systems

et al. 2021

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“…Hypercapnia has been found to attenuate cytokine production and oxygen free radical formation in mice subjected to alveolar stretch [5, 15]. Furthermore, hypercapnia markedly reduced apoptosis, oxidative stress, and inflammation in alveolar epithelial cells from high-pressure ventilation-stimulated rat lungs [20]. Hypercapnic acidosis (HCA) exerts anti-inflammatory effects in rabbits with endotoxin-induced lung injury [16].…”

Section: Biological Effects Of Hypercapnia—preclinical Studiesmentioning

confidence: 99%

The role of hypercapnia in acute respiratory failure

Morales-Quinteros

Camprubí-Rimblas

Bringué

et al. 2019

ICMx

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The biological effects and physiological consequences of hypercapnia are increasingly understood. The literature on hypercapnia is confusing, and at times contradictory. On the one hand, it may have protective effects through attenuation of pulmonary inflammation and oxidative stress. On the other hand, it may also have deleterious effects through inhibition of alveolar wound repair, reabsorption of alveolar fluid, and alveolar cell proliferation. Besides, hypercapnia has meaningful effects on lung physiology such as airway resistance, lung oxygenation, diaphragm function, and pulmonary vascular tree. In acute respiratory distress syndrome, lung-protective ventilation strategies using low tidal volume and low airway pressure are strongly advocated as these have strong potential to improve outcome. These strategies may come at a price of hypercapnia and hypercapnic acidosis. One approach is to accept it (permissive hypercapnia); another approach is to treat it through extracorporeal means. At present, it remains uncertain what the best approach is. Electronic supplementary material The online version of this article (10.1186/s40635-019-0239-0) contains supplementary material, which is available to authorized users.

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“…The biologic response to cyclic stretch occurs through mechanosensors that transmit signals from the deformed extracellular matrix to the interior of the cell [49,50]. Furthermore, hypercapnia markedly reduced apoptosis, oxidative stress and inflammation by inhibiting the downward activation of the signal-regulating kinase 1 JNK/p38 MAP-kinase pathway in alveolar epithelial cells [50]. 1).…”

Section: Ventilation-induced Lung Injury and Repairmentioning

confidence: 99%