Inflammatory response to cardiopulmonary bypass: mechanisms involved and possible therapeutic strategies.
BACKGROUND
Recent study of the inflammatory reactions occurring during and after cardiopulmonary bypass (CPB) has improved our understanding of the involvement of the inflammatory cascade in perioperative injury. However, the exact mechanisms of this complex response remain to be fully determined.


METHODS
Literature on the inflammatory response to CPB was reviewed to define current knowledge on the possible pathways and mediators involved, and to discuss recent developments of therapeutic interventions aimed at attenuating the inflammatory response to CPB.


RESULTS
CPB has been shown to induce complement activation, endotoxin release, leukocyte activation, the expression of adhesion molecules, and the release of many inflammatory mediators including oxygen-free radicals, arachidonic acid metabolites, cytokines, platelet-activating factor, nitric oxide, and endothelins. Therapies aimed at interfering with the inflammatory response include the administration of pharmacologic agents such as corticosteroids, aprotinin, and antioxidants, as well as modification of techniques and equipment by the use of heparin-coated CPB circuits, intraoperative leukocyte depletion, and ultrafiltration.


CONCLUSIONS
Improved understanding of the inflammatory reactions to CPB can lead to improved patient outcome by enabling the development of novel therapies aimed at limiting this response.
Wan
S
S
Department of Cardiac Surgery, University Hospital Erasme, Free University of Brussels, Belgium.
LeClerc
J L
JL
Vincent
J L
JL
D000305:Adrenal Cortex Hormones / Q000627:therapeutic use; D000925:Anticoagulants / Q000627:therapeutic use; D000975:Antioxidants / Q000627:therapeutic use; D007611:Aprotinin / Q000627:therapeutic use; D001095:Arachidonic Acids / Q000378:metabolism; D002315:Cardiopulmonary Bypass / Q000009:adverse effects* / Q000295:instrumentation; D015815:Cell Adhesion Molecules / Q000235:genetics; D003167:Complement Activation; D016207:Cytokines / Q000378:metabolism; D016232:Endothelins / Q000378:metabolism; D004731:Endotoxins / Q000378:metabolism; D004867:Equipment Design; D005609:Free Radicals / Q000378:metabolism; D015870:Gene Expression; D006493:Heparin / Q000627:therapeutic use; D006801:Humans; D007249:Inflammation / Q000378:metabolism / Q000503:physiopathology; D018836:Inflammation Mediators / Q000378:metabolism / Q000502:physiology; D007962:Leukocytes / Q000502:physiology; D007970:Leukopenia; D009569:Nitric Oxide / Q000378:metabolism; D010972:Platelet Activating Factor / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D015842:Serine Proteinase Inhibitors / Q000627:therapeutic use; D018746:Systemic Inflammatory Response Syndrome / Q000209:etiology* / Q000503:physiopathology / Q000628:therapy; D014462:Ultrafiltration
D000305:Adrenal Cortex Hormones; D000925:Anticoagulants; D000975:Antioxidants; D001095:Arachidonic Acids; D015815:Cell Adhesion Molecules; D016207:Cytokines; D016232:Endothelins; D004731:Endotoxins; D005609:Free Radicals; D018836:Inflammation Mediators; D010972:Platelet Activating Factor; D017382:Reactive Oxygen Species; D015842:Serine Proteinase Inhibitors; D009569:Nitric Oxide; D006493:Heparin; D007611:Aprotinin