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Cerebral inflammatory response during and after cardiac surgery.

Abstract

BACKGROUND AND OBJECTIVE

Neurological dysfunction is a common problem after cardiac surgery with cardiopulmonary bypass (CPB). Cerebral ischaemia associated with the use of CPB may result in a release of neuronal-ischaemic markers and a subsequent cerebral inflammatory response which may additionally release inflammatory cytokines. In order to locate the origin and to quantify the release of neuronal-ischaemic markers and cytokines we investigated arterial-cerebral venous concentration gradients during and after CPB in a clinical setting.

METHODS

In twenty-five patients scheduled for coronary artery bypass grafting surgery we measured the plasma concentration of neuron-specific enolase, S-100beta protein as well as interleukins (IL) IL-6, IL-8 and IL-10 from arterial and cerebral venous blood samples prior to surgery (baseline), during hypothermic CPB at 32 degrees C, after termination of bypass, as well as 2, 4 and 6 h after admission to the intensive care unit.

RESULTS

Arterial-cerebral venous concentration gradients of neuron-specific enolase, S-100beta, IL-6, IL-8 and IL-10 were neither detectable during nor after CPB. Compared to the baseline period, S-100beta and neuron-specific enolase significantly increased during hypothermic CPB. After termination of CPB, neuronal-ischaemic markers as well as cytokines were increased and remained elevated during the investigated time course without reaching baseline values.

CONCLUSIONS

Although we found an overall increase in plasma concentrations of neuronal-ischaemic markers, IL-6, IL-8 and IL-10 during and after CPB, arterial-cerebral venous gradients were not detectable for any of these parameters. Our results suggest that the increase of investigated parameters associated with the use of CPB are not primarily caused by a cerebral inflammatory response but rather reflect a release from other sources in the systemic circulation.

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  • Authors+Show Affiliations

    ,

    University of Göttingen, Department of Anaesthesiology, Göttingen, Germany. fmielck@gwdg.de

    , , , , , ,

    Source

    European journal of anaesthesiology 22:5 2005 May pg 347-52

    MeSH

    Aged
    Analysis of Variance
    Biomarkers
    Brain
    Cardiac Surgical Procedures
    Coronary Artery Bypass
    Encephalitis
    Humans
    Inflammation Mediators
    Interleukins
    Intraoperative Complications
    Male
    Middle Aged
    Phosphopyruvate Hydratase
    Postoperative Complications
    S100 Proteins
    Time Factors

    Pub Type(s)

    Journal Article

    Language

    eng

    PubMed ID

    15918382

    Citation

    TY - JOUR T1 - Cerebral inflammatory response during and after cardiac surgery. AU - Mielck,F, AU - Ziarkowski,A, AU - Hanekop,G, AU - Armstrong,V W, AU - Hilgers,R, AU - Weyland,A, AU - Quintel,M, AU - Sonntag,H, PY - 2005/5/28/pubmed PY - 2005/9/28/medline PY - 2005/5/28/entrez SP - 347 EP - 52 JF - European journal of anaesthesiology JO - Eur J Anaesthesiol VL - 22 IS - 5 N2 - BACKGROUND AND OBJECTIVE: Neurological dysfunction is a common problem after cardiac surgery with cardiopulmonary bypass (CPB). Cerebral ischaemia associated with the use of CPB may result in a release of neuronal-ischaemic markers and a subsequent cerebral inflammatory response which may additionally release inflammatory cytokines. In order to locate the origin and to quantify the release of neuronal-ischaemic markers and cytokines we investigated arterial-cerebral venous concentration gradients during and after CPB in a clinical setting. METHODS: In twenty-five patients scheduled for coronary artery bypass grafting surgery we measured the plasma concentration of neuron-specific enolase, S-100beta protein as well as interleukins (IL) IL-6, IL-8 and IL-10 from arterial and cerebral venous blood samples prior to surgery (baseline), during hypothermic CPB at 32 degrees C, after termination of bypass, as well as 2, 4 and 6 h after admission to the intensive care unit. RESULTS: Arterial-cerebral venous concentration gradients of neuron-specific enolase, S-100beta, IL-6, IL-8 and IL-10 were neither detectable during nor after CPB. Compared to the baseline period, S-100beta and neuron-specific enolase significantly increased during hypothermic CPB. After termination of CPB, neuronal-ischaemic markers as well as cytokines were increased and remained elevated during the investigated time course without reaching baseline values. CONCLUSIONS: Although we found an overall increase in plasma concentrations of neuronal-ischaemic markers, IL-6, IL-8 and IL-10 during and after CPB, arterial-cerebral venous gradients were not detectable for any of these parameters. Our results suggest that the increase of investigated parameters associated with the use of CPB are not primarily caused by a cerebral inflammatory response but rather reflect a release from other sources in the systemic circulation. SN - 0265-0215 UR - https://www.unboundmedicine.com/medline/citation/15918382/Cerebral_inflammatory_response_during_and_after_cardiac_surgery_ L2 - http://ovidsp.ovid.com/ovidweb.cgi?T=JS&PAGE=linkout&SEARCH=15918382.ui ER -