Inflammatory response to cardiopulmonary bypass.
Other Article (Journal 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
International Standard Serial Number (ISSN)
- 0003-4975
Digital Object Identifier (DOI)
- 10.1016/s0003-4975(02)04701-x
Language
- eng
Conference Location
- Netherlands