Document Detail


Exacerbation of systemic inflammation and increased cerebral infarct volume with cardiopulmonary bypass after focal cerebral ischemia in the rat.
MedLine Citation:
PMID:  20236669     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: Stroke remains a significant contributor to morbidity and mortality after cardiac surgery. Cardiopulmonary bypass is known to induce a significant inflammatory response, which could adversely influence outcomes. We hypothesized that cardiopulmonary bypass, through an enhanced systemic inflammatory response, might affect outcomes after focal cerebral ischemia. METHODS: Wistar rats (275-300 g) were anesthetized, surgically prepared for cardiopulmonary bypass and right middle cerebral artery occlusion, and randomly allocated to 2 groups: focal cerebral ischemia alone (n = 9) and focal cerebral ischemia combined with normothermic cardiopulmonary bypass (n = 8). Serum cytokines (tumor necrosis factor alpha and interleukins 1beta, 6, and 10) were measured at baseline, at end of bypass, and at 2, 6, and 24 hours after bypass. On postoperative day 3, animals underwent neurologic testing, after which the brains were prepared for assessment of cerebral infarct volume. Data were compared between groups by Mann-Whitney U test. RESULTS: Compared with the ischemia-alone group, the ischemia plus bypass group had significantly higher levels of circulating tumor necrosis factor alpha and interleukins 1beta and 10 at the end of bypass and 2 hours after bypass. In addition, the ischemia plus bypass animals had larger total cerebral infarct volumes (286 +/- 125 mm(3)) than did those with ischemia alone (144 +/- 85 mm(3), P = .0124). CONCLUSIONS: Cardiopulmonary bypass increased cerebral infarct size after focal cerebral ischemia in rats. This worsening of outcome may in part be related to an augmented inflammatory response that accompanies cardiopulmonary bypass.
Authors:
H Mayumi Homi; Wilbert L Jones; Fellery de Lange; G Burkhard Mackensen; Hilary P Grocott
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-03-16
Journal Detail:
Title:  The Journal of thoracic and cardiovascular surgery     Volume:  140     ISSN:  1097-685X     ISO Abbreviation:  J. Thorac. Cardiovasc. Surg.     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-08-20     Completed Date:  2010-09-20     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0376343     Medline TA:  J Thorac Cardiovasc Surg     Country:  United States    
Other Details:
Languages:  eng     Pagination:  660-6, 666.e1     Citation Subset:  AIM; IM    
Copyright Information:
2010 The American Association for Thoracic Surgery. Published by Mosby, Inc. All rights reserved.
Affiliation:
Division of Cardiothoracic Anesthesiology and Critical Care Medicine, Department of Anesthesiology, Duke University Medical Center, Durham, NC, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Behavior, Animal
Biological Markers / blood
Brain Ischemia / complications*,  immunology,  pathology,  physiopathology
Cardiopulmonary Bypass / adverse effects*
Disease Models, Animal
Infarction, Middle Cerebral Artery / etiology*,  immunology,  pathology,  physiopathology
Inflammation Mediators / blood
Interleukin-10 / blood
Interleukin-1beta / blood
Interleukin-6 / blood
Male
Motor Activity
Rats
Rats, Wistar
Systemic Inflammatory Response Syndrome / etiology*,  immunology
Time Factors
Tumor Necrosis Factor-alpha / blood
Up-Regulation
Chemical
Reg. No./Substance:
0/Biological Markers; 0/Inflammation Mediators; 0/Interleukin-1beta; 0/Interleukin-6; 0/Tumor Necrosis Factor-alpha; 130068-27-8/Interleukin-10

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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