Inflammatory response to cardiopulmonary bypass.

Published

Other Article (Review)

Inflammation in cardiac surgical patients is produced by complex humoral and cellular interactions with numerous pathways including activation, generation, or expression of thrombin, complement, cytokines, neutrophils, adhesion molecules, mast cells, and multiple inflammatory mediators. Because of the redundancy of the inflammatory cascades, profound amplification occurs to produce multiorgan system dysfunction that can manifest as coagulopathy, respiratory failure, myocardial dysfunction, renal insufficiency, and neurocognitive defects. Coagulation and inflammation are also closely linked through networks of both humoral and cellular components including proteases of the clotting and fibrinolytic cascades, including tissue factor. Vascular endothelial cells also mediate inflammation and the cross talk between coagulation and inflammation. Novel antiinflammatory agents inhibit these processes by several mechanisms such as preventing proteolysis of the protease-activated receptor (aprotinin), inhibiting complement-mediated injury (pexelizumab), or inhibiting contact activation (kallikrein inhibitors). Surgery alone also activates specific hemostatic responses, activation of immune mechanisms, and inflammatory response mediated by the release of various cytokines and chemokines. Novel agents are under investigation to further improve outcomes in cardiac surgical patients.

Full Text

Duke Authors

Cited Authors

  • Levy, JH; Tanaka, KA

Published Date

  • February 2003

Published In

Volume / Issue

  • 75 / 2

Start / End Page

  • S715 - S720

PubMed ID

  • 12607717

Pubmed Central ID

  • 12607717

Electronic International Standard Serial Number (EISSN)

  • 1552-6259

International Standard Serial Number (ISSN)

  • 0003-4975

Digital Object Identifier (DOI)

  • 10.1016/s0003-4975(02)04701-x

Language

  • eng