- Meeting abstract
- Open Access
sCD14, IL-6 and TNF-receptors, but not IL-1, IL-8 or TNF-α are elevated in plasma of patients undergoing high risk coronary angioplasty with cardiopulmonary support
© Current Science Ltd 1999
- Published: 16 March 2000
- Coronary Artery Disease
- Cardiopulmonary Bypass
- Antiinflammatory Cytokine
- National Registry
- Cytokine Release
The cardiopulmonary bypass (CPB) is discussed as a potential trigger of cytokine release. Here we determined a not investigated spectrum of pro- and antiinflammatory cytokines in high risk patients undergoing CPB-PTCA.
Patients with coronary artery disease (n = 3) with a high risk of coronary intervention according to the `National registry for supported angioplasty, 1994' undergoing CPB-supported PTCA were examined. Interleukin 1α (IL-1α), IL-1β, IL-1 receptor antagonist (IL-1ra), Tumor-necrosis-factor-α (TNF-α), soluble TNF-Receptors (TNF-R-p55: TNF-R-p75), IL-6, IL-8, IL-10 and soluble CD14 (sCD14) levels were measured in specific commercially available ELISA-Tests.
We detected no significant levels of IL-1α, IL-1β, IL-8 and TNF-α during CPB support. IL-1ra levels were increased. IL-6 levels increased measurable starting 30 min after begin of CPB with peak values of 20-60 pg/ml between 3 and 12 h. One patient showed significant levels of IL-10, this patient expressed the lowest level and shortest kinetic of IL-6 production and more pronounced TNFα -receptor levels, although TNF-receptor levels increased in all patients. sCD14 raised continously in all 3 patients to a maximum of 7 ng/ml followed by a plateau for more than 5 days.
In this study we compared the cytokine levels of patients undergoing high risk coronary angioplasty with CPB-support. There were no findings to show a significant relation of IL-1α, IL-1β, IL-8 and TNF-α to the inflammatory response after CPB-PTCA - this might be a sign for other mechanisms than systemic activation of monocytes by endotoxin may be involved. IL-6 as a marker of the degree of systemic inflammatory reaction increased significantly. We suggest, the mayor source of this increase of IL-6 levels is the CPB-support. IL-6 release might be inhibited by IL-10 production.