Hyperglycaemia and apoptosis of microglial cells in human septic shock.

Details

Serval ID
serval:BIB_A71ECB99BD75
Type
Article: article from journal or magazin.
Collection
Publications
Title
Hyperglycaemia and apoptosis of microglial cells in human septic shock.
Journal
Critical Care (london, England)
Author(s)
Polito A., Brouland J.P., Porcher R., Sonneville R., Siami S., Stevens R.D., Guidoux C., Maxime V., de la Grandmaison G.L., Chrétien F.C., Gray F., Annane D., Sharshar T.
ISSN
1466-609X (Electronic)
ISSN-L
1364-8535
Publication state
Published
Issued date
2011
Peer-reviewed
Oui
Volume
15
Number
3
Pages
R131
Language
english
Notes
Publication types: Journal ArticlePublication Status: ppublish
Abstract
INTRODUCTION: The effect of hyperglycaemia on the brain cells of septic shock patients is unknown. The objective of this study was to evaluate the relationship between hyperglycaemia and apoptosis in the brains of septic shock patients.
METHODS: In a prospective study of 17 patients who died from septic shock, hippocampal tissue was assessed for neuronal ischaemia, neuronal and microglial apoptosis, neuronal Glucose Transporter (GLUT) 4, endothelial inducible Nitric Oxide Synthase (iNOS), microglial GLUT5 expression, microglial and astrocyte activation. Blood glucose (BG) was recorded five times a day from ICU admission to death. Hyperglycaemia was defined as a BG 200 mg/dL g/l and the area under the BG curve (AUBGC) > 2 g/l was assessed.
RESULTS: Median BG over ICU stay was 2.2 g/l. Neuronal apoptosis was correlated with endothelial iNOS expression (rho = 0.68, P = 0.04), while microglial apoptosis was associated with AUBGC > 2 g/l (rho = 0.70; P = 0.002). Neuronal and microglial apoptosis correlated with each other (rho = 0.69, P = 0.006), but neither correlated with the duration of septic shock, nor with GLUT4 and 5 expression. Neuronal apoptosis and ischaemia tended to correlate with duration of hypotension.
CONCLUSIONS: In patients with septic shock, neuronal apoptosis is rather associated with iNOS expression and microglial apoptosis with hyperglycaemia, possibly because GLUT5 is not downregulated. These data provide a mechanistic basis for understanding the neuroprotective effects of glycemic control.
Keywords
Aged, Apoptosis, Blood Glucose/analysis, Brain/metabolism, Brain/pathology, Female, Humans, Hyperglycemia, Male, Microglia/metabolism, Microglia/pathology, Middle Aged, Prospective Studies, Shock, Septic/metabolism, Shock, Septic/pathology
Pubmed
Web of science
Open Access
Yes
Create date
13/10/2015 10:08
Last modification date
20/08/2019 15:11
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