Hypercapnia attenuates ventilator-induced lung injury through vagus nerve activation

Xia, Wenfang; Li, Guang; Zhou, Pan; Zhou, Qingshan

doi:10.1590/s0102-865020190090000002

Cited by 2 publications

(4 citation statements)

References 28 publications

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“…It has been widely believed that the injuries induced by inappropriate MV, such as barometric trauma, volume trauma, and atelectasis, are likely to progress into local inflammatory imbalance or even systemic inflammatory response, which is featured by the cytokines production and pulmonary edema, ultimately leading to impaired lung function. [ 39 ] VILI has been revealed to consistently lead to the release of inflammatory indicators and cytokines. A marked augmentation of IL‐1, IL‐6, and TNF‐α was detected in BALF after conventional MV over 36 h in patients.…”

Section: Discussionmentioning

confidence: 99%

BMSCs mediates endothelial cell autophagy by upregulating miR‐155‐5p to alleviate ventilator‐induced lung injury

Lin

Luo

et al. 2022

J Biochem & Molecular Tox

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In this study, we explored to detect the effects and mechanism of bonemarrow-derived mesenchymal stem cells (BMSCs) on ventilator-induced lung injury (VILI). We transplanted BMSCs in mice and then induced VILI using mechanical ventilation (MV) treatment. The pathological changes, the content of PaO 2 and PaCO 2 , wet/dry weight ratio (W/D) of the lung, levels of tumor necrosis factor-α and interleukin-6 in bronchoalveolar lavage fluid, and apoptosis were detected. The autophagy-associated factor p62, LC3, and Beclin-1 expression were analyzed by western blot. The quantitative polymerase chain reaction was applied to detect abnormally expressed microRNAs, including miR-155-5p. Subsequently, we overexpressed miR-155-5p in VILI mice to detect the effects of miR-155-5p on MV-induced lung injury. Then, we carried out bioinformatics analysis to verify the BMSCs-regulated miR-155-5p that target messenger RNA. It was observed that BMSCs transplantation mitigated the severity of VILI in mice. BMSCs transplantation reduced lung inflammation, strengthened the arterial oxygen partial pressure, and reduced apoptosis and the W/D of the lung. BMSCs promoted autophagy of pulmonary endothelial cells accompanied by decreased p62 and increased LC3 II/I and Beclin-1. BMSCs increased the levels of miR-155-5p in VILI mice. Overexpression of miR-155-5p alleviated lung injury in VILI mice following reduced apoptosis and increased autophagy. Finally, TAB2 was identified as a downstream target of miR-155-5p and regulated by miR-155-5p. BMSCs may protect lung tissues from MV-induced injury, inhibit lung inflammation, promote autophagy through upregulating of miR-155-5p.

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Section: Discussionmentioning

confidence: 99%

BMSCs mediates endothelial cell autophagy by upregulating miR‐155‐5p to alleviate ventilator‐induced lung injury

Lin

Luo

et al. 2022

J Biochem & Molecular Tox

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“…A study by Xia et al recently identified that HC (FICO 2 0.05) enhanced vagus nerve activity to produce therapeutic effects in the lung [30]. They found that performing a vagotomy abolished the protective effects that HC provided which consisted of reduced MPO activity, reduced BAL cytokines, protein and cell count, and reduced histologic injury scores [30]. Otulakowski et al showed that HC (FICO 2 0.12) inhibits stretch-mediated activation of p44/42 MAPK signalling in alveolar epithelial cells which occurs through the inhibition of the metalloprotease ADAM17 [27].…”

Section: The Effects Of Hypercapnia In Preclinical Models Of Acute Lumentioning

confidence: 99%

“…[ 29 ] VILI in rats HC (FICO 2 0.5) ↑ compliance, ↓ MPO activity ↓ BAL cytokines ↓ cell counts ↓ BAL protein ↓ histological injury score ↑ efferent vagus nerve activity Xia et al . [ 30 ] reperfusion isolated buffer-perfused lung in rabbits HCA (FICO 2 0.25) ↓ pulmonary microvascular permeability ↓ capillary and pulmonary artery pressures Shibata et al . [ 31 ] lung reperfusion in rabbits HC (FICO 2 0.12) ↓ pulmonary oedema ↓ apoptosis ↑ oxygenation ↓ BAL TNF-α ↓ lung tissue 8-isoprostane ↓ nitrotyrosine Laffey et al .…”

Section: The Effects Of Hypercapnia In Preclinical Models Of Acute Lumentioning

confidence: 99%

“…A study by Xia et al . recently identified that HC (FICO 2 0.05) enhanced vagus nerve activity to produce therapeutic effects in the lung [ 30 ]. They found that performing a vagotomy abolished the protective effects that HC provided which consisted of reduced MPO activity, reduced BAL cytokines, protein and cell count, and reduced histologic injury scores [ 30 ].…”

Section: The Effects Of Hypercapnia In Preclinical Models Of Acute Lumentioning

confidence: 99%

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Hypercapnia in the critically ill: insights from the bench to the bedside

et al. 2021

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Carbon dioxide (CO 2 ) has long been considered, at best, a waste by-product of metabolism, and at worst, a toxic molecule with serious health consequences if physiological concentration is dysregulated. However, clinical observations have revealed that ‘permissive’ hypercapnia, the deliberate allowance of respiratory produced CO 2 to remain in the patient, can have anti-inflammatory effects that may be beneficial in certain circumstances. In parallel, studies at the cell level have demonstrated the profound effect of CO 2 on multiple diverse signalling pathways, be it the effect from CO 2 itself specifically or from the associated acidosis it generates. At the whole organism level, it now appears likely that there are many biological sensing systems designed to respond to CO 2 concentration and tailor respiratory and other responses to atmospheric or local levels. Animal models have been widely employed to study the changes in CO 2 levels in various disease states and also to what extent permissive or even directly delivered CO 2 can affect patient outcome. These findings have been advanced to the bedside at the same time that further clinical observations have been elucidated at the cell and animal level. Here we present a synopsis of the current understanding of how CO 2 affects mammalian biological systems, with a particular emphasis on inflammatory pathways and diseases such as lung specific or systemic sepsis. We also explore some future directions and possibilities, such as direct control of blood CO 2 levels, that could lead to improved clinical care in the future.

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Hypercapnia attenuates ventilator-induced lung injury through vagus nerve activation

Cited by 2 publications

References 28 publications

BMSCs mediates endothelial cell autophagy by upregulating miR‐155‐5p to alleviate ventilator‐induced lung injury

BMSCs mediates endothelial cell autophagy by upregulating miR‐155‐5p to alleviate ventilator‐induced lung injury

Hypercapnia in the critically ill: insights from the bench to the bedside

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