H-Index
79
Scimago Lab
powered by Scopus
JCR
Clarivate
Analytics
12%
Acceptance
Rate
call: +1.631.470.9640
Mon-Fri 10 am - 2 pm EST

Logo

Medical Science Monitor Basic Research
AmJCaseRep

Annals
ISI-Home

eISSN: 1643-3750

Get your full text copy in PDF

Role of the Sympathetic Nervous System and Spleen in Experimental Stroke-Induced Immunodepression

Fu-Ling Yan, Jin-Hua Zhang

(Department of Neurology, Zhong-Da Hospital, Southeast University, Nanjing, China (mainland))

Med Sci Monit 2014; 20:2489-2496

DOI: 10.12659/MSM.890844


Background: The mechanism of stroke-induced immunodepression syndrome (SIDS) remains uncertain. Some studies suggest that hyperactivation of the sympathetic nervous system (SNS) may be the key factor underlying SIDS. Catecholamines impair early lymphocyte response, which can increase the risk of stroke-associated infection (SAI).
Material and Methods: Our study focused on dynamic changes of metanephrine (MN), normetanephrine (NMN), cytokines, and spleen volume in the rat middle cerebral artery occlusion (MCAO) model.
Results: After MCAO, there is hyperactivation of SNS and pro-/anti-inflammatory imbalance, indicating systemic immunodepression. In addition, rat spleen size was reduced. Correlation analysis indicated that MCAO-induced spleen size reduction correlated with the changes in MN, NMN, and cytokines. Blocking SNS with propranolol can partly reverse the immunodepression and the reduction in spleen volume.
Conclusions: Taken together, these findings suggest that acute ischemic stroke induces over-activation of the SNS, which lowers the threshold of infection and increases the risk of infection.

This paper has been published under Creative Common Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) allowing to download articles and share them with others as long as they credit the authors and the publisher, but without permission to change them in any way or use them commercially.
I agree