Potential therapeutic value of dexmedetomidine in COVID-19 patients admitted to ICU

Zhao, Hailin; Davies, R. G.; Ma, Daqing

doi:10.1016/j.bja.2020.09.031

Cited by 29 publications

(35 citation statements)

References 12 publications

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“…[2][3][4][5][6] Based on studies investigating its effects in reducing sepsis-related lung injury and ischaemia-reperfusion injury of heart, kidney, brain, and intestine (organs commonly affected in COVID-19), 7 and based on the mechanistic models of COVID-19 pathogenesis, [8][9][10][11] we suggest that dexmedetomidine may have therapeutic potential in COVID-19. Our hypothesis is supported by a case report of improved oxygenation with dexmedetomidine in a COVID-19 patient, 12 as well as by another encouraging report 13 .…”

supporting

confidence: 73%

“…Dexmedetomidine-mediated activation of cholinergic pathways and decreased sympathetic tone confers additional cytoprotective and antiinflammatory benefits. 13 Use of dexmedetomidine for sedation in COVID-19 may have a theoretical advantage of skewing the immune response away from Th17 19 which has been linked with immunopathogenesis of severe COVID-19 pneumonia 20 . Additionally, dexmedetomidine increases expression of natural killer cells, B-cells, CD4 + T cells, and the ratios of CD4+:CD8+…”

Section: J O U R N a L P R E -P R O O Fmentioning

confidence: 99%

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Dexmedetomidine: another arrow in the quiver to fight COVID-19 in intensive care units

Jain¹,

Lamperti²,

Doyle

2021

British Journal of Anaesthesia

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supporting

confidence: 73%

Section: J O U R N a L P R E -P R O O Fmentioning

confidence: 99%

Dexmedetomidine: another arrow in the quiver to fight COVID-19 in intensive care units

Jain¹,

Lamperti²,

Doyle

2021

British Journal of Anaesthesia

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“…However, it is acceptable in general because the drug dose for rodents is usually 7 times higher than human use. Secondly, the current study is a physiological and pharmacological study, more cellular and molecular mechanistic studies with this experimental setting are needed in future for better understanding the clinical applications of Dex in sepsis and even virus infections, such as SARS-CoV-2, that we are currently facing (Zhao, Davies, and Ma 2021).…”

Section: Discussionmentioning

confidence: 99%

The Role of Vagus Nerve on Dexmedetomidine Induced Survival and Lung Protection in a Sepsis Model in Rats.

et al. 2021

Preprint

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BackgroundSepsis often results in acute lung injury (ALI). Sedative dexmedetomidine (Dex) was reported to protect cells and organs due to its direct cellular effects. This study aims to investigate the role of vagus nerves on Dex induced lung protection in a model of lipopolysaccharide (LPS)-induced ALI in rats. MethodsThe bilateral cervical vagus nerve of male Sprague-Dawley rats was sectioned or just exposed without section as sham surgery. The ALI was induced by intraperitoneal injection of LPS (1 or 10 mg/kg). After LPS administration, Dex antagonist yohimbine (YOH) (1 mg/kg) and/or Dex (25 μg/kg) was injected intraperitoneally at 0, 4, 8 and 12 hours to rats with or without vagotomy. The severity of ALI was determined with survival curve analysis and lung pathological scores of haematoxylin and eosin (H-E) staining sections. The plasma concentrations of interleukin 1beta (IL-1β), tumour necrosis factor-alpha (TNF-α), catecholamine (CA) and acetylcholine (Ach) were measured with enzyme-linked immunosorbent assay (ELISA). ResultsThe median survival time of LPS-induced ALI rats was significantly prolonged by Dex (22 hours, 50% CI, [31.25, 90.63]) compared that in the LPS group (14 hours, 50% CI, [18.75, 81.25], P < 0.05), and the acute lung injury score was significantly reduced by Dex (6.5, 50% CI, [5.75, 7.5] vs 11.5, 50% CI, [10.75, 12.50] in the LPS group, P < 0.01). However, these protective effects of Dex were significantly reduced by either YOH administration or vagotomy. Dex significantly decreased LPS-induced plasma IL-1β (pg/ml) (20.75 ± 0.78 vs. 30.22 ± 2.62, P < 0.01), TNF-α (pg/ml) (205.30 ± 9.39 vs. 273.40 ± 14.50, P < 0.01), and CA (pg/ml) (825.70 ± 43.46 vs. 1188.00 ± 64.40, P < 0.01) but increased the secretion of Ach (pg/ml) (507.20 ± 49.52 vs. 296.50 ± 62.44, P < 0.01); these effects of Dex was partially abolished by vagotomy. ConclusionsOur data suggested that Dex increased vagal nerve tone which partially contributed to its anti-inflammatory and lung protective effects. The indirect anti-inflammation and direct cytoprotection of Dex are likely through high vagal nerve tone and α 2 -adrenoceptor activation, respectively.

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“…7 To conclude, the aforementioned experience highlights the present-day relevance of a sound perioperative risk comprehension, consent appropriate to the level of planned surgical intervention to be equally backed by a case-based approach for the anticipation, and the attenuation of the second inflammatory hit aimed at ameliorating the overall severity of the postoperative disease. 8,9 Meanwhile, prudent feasible suggestions from our colleagues on minimizing such perioperative circumstances are more than welcome.…”

mentioning

confidence: 99%

Postoperative inflammation to “hyper”‐inflammation: cryptic COVID‐19 connections!

Magoon

ItiShri

Kohli

et al. 2021

Pediatric Anesthesia

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Potential therapeutic value of dexmedetomidine in COVID-19 patients admitted to ICU

Cited by 29 publications

References 12 publications

Dexmedetomidine: another arrow in the quiver to fight COVID-19 in intensive care units

Dexmedetomidine: another arrow in the quiver to fight COVID-19 in intensive care units

The Role of Vagus Nerve on Dexmedetomidine Induced Survival and Lung Protection in a Sepsis Model in Rats.

Postoperative inflammation to “hyper”‐inflammation: cryptic COVID‐19 connections!

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