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This article is part of the supplement: International Symposium on the Pathophysiology of Cardiopulmonary Bypass .

Meeting abstract

Acute phase response following cardiopulmonary bypass: impact of corticoid therapy

E Ebert, R Bauernschmitt, R Lange and S Hagl

Department Cardiac Surgery, University of Heidelberg, INF 110, 69120 Heidelberg

from International Symposium on the Pathophysiology of Cardiopulmonary Bypass
Aachen, Germany. 12 December 1998

Critical Care 1999, 3(Suppl A):P24doi:10.1186/cc335

The electronic version of this abstract is the complete one and can be found online at: http://ccforum.com/content/3/SA/P24

Published: 2 March 1999

© 1999 Current Science Ltd

Full text

Cardiac surgery with cardiopulmonary bypass (CPB) leads to an acute phase response characterized by the synthesis of proinflammatory cytokines and activation of the complement system. The following study was performed to analyse the influence of corticoid-premedication on acute phase response and clinical course of the patients.

Twenty-one male patients with three-vessel disease and normal or moderately impaired left ventricular function undergoing elective or urgent CABG-surgery were included. 10 patients received 125 mg of dexamethasone in addition to the standard premedication regimen, while 11 patients served as controls. Blood samples were drawn preoperatively, 10 min after termination of CPB and 4 h after CPB to determine the levels of interleukin-6 (IL-6), interleukin-8, tumor-necrosis-factor (TNF) and the anaphylatoxin C3a.

There was a marked increase of cytokines and activation of the complement system in all patients following the surgical intervention. Corticoid treatment resulted in a significant reduction of IL-6, IL-8 and TNF 10 min and 4 h following CPB. The activation of complement did not differ in both patients groups.

Pretreatment with corticosteroids results in a significant suppression of the cytokine response following CPB, which, however, does not have a major impact on the clinical course. Further studies have to analyse, whether inhibition of the acute phase response may lead to clinical improvements in selected high-risk patients.

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