Remote ischaemic preconditioning does not modulate the systemic inflammatory response or renal tubular stress biomarkers after endotoxaemia in healthy human volunteers: a single-centre, mechanistic, randomised controlled trial.
cytokine
endotoxaemia
immunity
innate
ischaemic preconditioning
lipopolysaccharides
renal tubular stress
systemic inflammatory response
Journal
British journal of anaesthesia
ISSN: 1471-6771
Titre abrégé: Br J Anaesth
Pays: England
ID NLM: 0372541
Informations de publication
Date de publication:
Aug 2019
Aug 2019
Historique:
received:
09
01
2019
revised:
15
02
2019
accepted:
02
03
2019
pubmed:
16
5
2019
medline:
8
8
2019
entrez:
16
5
2019
Statut:
ppublish
Résumé
Remote ischaemic preconditioning (RIPC) consists of repeated cycles of limb ischaemia and reperfusion, which may reduce perioperative myocardial ischaemic damage and kidney injury. We hypothesised that RIPC may be beneficial by attenuating the systemic inflammatory response. We investigated whether RIPC affects the response in humans to bacterial endotoxin (lipopolysaccharide [LPS]) by measuring plasma cytokines and renal cell-cycle arrest mediators, which reflect renal tubular stress. Healthy male volunteers were randomised to receive either daily RIPC for 6 consecutive days (RIPC In both RIPC groups, RIPC alone increased [TIMP2]*[IGFBP7]. LPS administration resulted in fever, flu-like symptoms, and haemodynamic alterations. Plasma cytokine concentrations increased profoundly during endotoxaemia (control group: tumor necrosis factor alpha [TNF-α] from 14 [9-16] pg ml RIPC neither modulated systemic cytokine release nor attenuated inflammation-induced tubular stress after LPS. However, RIPC alone induced renal markers of cell-cycle arrest. NCT02602977.
Sections du résumé
BACKGROUND
BACKGROUND
Remote ischaemic preconditioning (RIPC) consists of repeated cycles of limb ischaemia and reperfusion, which may reduce perioperative myocardial ischaemic damage and kidney injury. We hypothesised that RIPC may be beneficial by attenuating the systemic inflammatory response. We investigated whether RIPC affects the response in humans to bacterial endotoxin (lipopolysaccharide [LPS]) by measuring plasma cytokines and renal cell-cycle arrest mediators, which reflect renal tubular stress.
METHODS
METHODS
Healthy male volunteers were randomised to receive either daily RIPC for 6 consecutive days (RIPC
RESULTS
RESULTS
In both RIPC groups, RIPC alone increased [TIMP2]*[IGFBP7]. LPS administration resulted in fever, flu-like symptoms, and haemodynamic alterations. Plasma cytokine concentrations increased profoundly during endotoxaemia (control group: tumor necrosis factor alpha [TNF-α] from 14 [9-16] pg ml
CONCLUSIONS
CONCLUSIONS
RIPC neither modulated systemic cytokine release nor attenuated inflammation-induced tubular stress after LPS. However, RIPC alone induced renal markers of cell-cycle arrest.
CLINICAL TRIAL REGISTRATION
BACKGROUND
NCT02602977.
Identifiants
pubmed: 31084985
pii: S0007-0912(19)30242-9
doi: 10.1016/j.bja.2019.03.037
pmc: PMC6676055
pii:
doi:
Substances chimiques
Biomarkers
0
Banques de données
ClinicalTrials.gov
['NCT02602977']
Types de publication
Journal Article
Randomized Controlled Trial
Langues
eng
Pagination
177-185Commentaires et corrections
Type : CommentIn
Informations de copyright
Copyright © 2019 British Journal of Anaesthesia. Published by Elsevier Ltd. All rights reserved.
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