Autonomic Disbalance During Systemic Inflammation is Associated with Oxidative Stress Changes in Sepsis Survivor Rats.

Szczegóły
Abstrakt

Tytuł:: Autonomic Disbalance During Systemic Inflammation is Associated with Oxidative Stress Changes in Sepsis Survivor Rats.
Autorzy:: Amorim MR; Dental School of Ribeirão Preto, University of São Paulo, Avenida Do Café s/n, São Paulo, 14040-904, Ribeirão Preto, Brazil. .; Division of Pulmonary and Critical Care Medicine, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD, USA. .
de Jesus AA; Medical School of Ribeirão Preto, University of São Paulo, Ribeirão Preto, São Paulo, Brazil.
Santos-Junior NN; Medical School of Ribeirão Preto, University of São Paulo, Ribeirão Preto, São Paulo, Brazil.
Rocha MJA; Dental School of Ribeirão Preto, University of São Paulo, Avenida Do Café s/n, São Paulo, 14040-904, Ribeirão Preto, Brazil.
Nogueira JE; School of Physical Education and Sports of Ribeirão Preto, University of São Paulo, Ribeirão Preto, São Paulo, Brazil.
Batalhão ME; Nursing School of Ribeirão Preto, University of São Paulo, Ribeirão Preto, São Paulo, 14040-902, Brazil.
Cárnio EC; Nursing School of Ribeirão Preto, University of São Paulo, Ribeirão Preto, São Paulo, 14040-902, Brazil.
Branco LGS; Dental School of Ribeirão Preto, University of São Paulo, Avenida Do Café s/n, São Paulo, 14040-904, Ribeirão Preto, Brazil. .
Źródło:: Inflammation [Inflammation] 2022 Jun; Vol. 45 (3), pp. 1239-1253. Date of Electronic Publication: 2022 Jan 04.
Typ publikacji:: Journal Article
Język:: English
Imprint Name(s):: Publication: 1999- : New York, NY : Kluwer Academic/Plenum Publishers
Original Publication: New York, Plenum Press.
MeSH Terms:: Lipopolysaccharides*/pharmacology
Sepsis*
Animals ; Cecum/metabolism ; Disease Models, Animal ; Inflammation/etiology ; Male ; Oxidative Stress ; Rats ; Rats, Wistar ; Superoxide Dismutase/metabolism ; Survivors ; Thiobarbituric Acid Reactive Substances
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Grant Information:: #2016/17681-9 fapesp; #2017/09878-0 fapesp
Contributed Indexing:: Keywords: blood pressure; cecal ligation and puncture; endotoxin.; septic shock
Substance Nomenclature:: 0 (Lipopolysaccharides)
0 (Thiobarbituric Acid Reactive Substances)
EC 1.15.1.1 (Superoxide Dismutase)
Entry Date(s):: Date Created: 20220104 Date Completed: 20220516 Latest Revision: 20220531
Update Code:: 20240104
DOI:: 10.1007/s10753-021-01617-6
PMID:: 34981315
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Sepsis affects 31.5 million people worldwide. It is characterized by an intense drop in blood pressure driving to cardiovascular morbidity and mortality. Modern supportive care has increased survival in patients; however, after experiencing sepsis, several complications are observed, which may be potentiated by new inflammatory events. Nevertheless, the interplay between sepsis survivors and a new immune challenge in cardiovascular regulation has not been previously defined. We hypothesized that cecal ligation and puncture (CLP) cause persistent cardiovascular dysfunctions in rats as well as changes in autonomic-induced cardiovascular responses to lipopolysaccharide (LPS). Male Wistar rats had mean arterial pressure (MAP) and heart rate (HR) recorded before and after LPS or saline administration to control or CLP survivor rats. CLP survivor rats had similar baseline MAP and HR when compared to control. LPS caused a drop in MAP accompanied by tachycardia in control, while CLP survivor rats had a noteworthy enhanced MAP and a blunted tachycardia. LPS-induced hemodynamic changes were related to an autonomic disbalance to the heart and resistance vessels that were expressed as an increased low- and high-frequency power of pulse interval in CLP survivors after saline and enhancement in the low-frequency power of systolic arterial pressure in control rats after LPS. LPS-induced plasma interferon γ, but not interleukin-10 surges, was blunted in CLP survivor rats. To further access whether or not LPS-induced autonomic disbalance in CLP survivor rats was associated with oxidative stress dysregulation, superoxide dismutase (SOD) activity and thiobarbituric acid reactive substances (TBARS) plasma levels changes were measured. LPS-induced oxidative stress was higher in CLP survivor rats. These findings indicate that key changes in hemodynamic regulation of CLP survivors rats take place in response to LPS that are associated with oxidative stress changes, i.e., reduced SOD activity and increased TBARS levels.
(© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

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