Inflammatory response to cardiopulmonary bypass using two different types of                 heparin-coated extracorporeal circuits

Baufreton, Christophe; Moczar, M; Intrator, L; Jansen, Piet; Velthuis, Henk te; Besnerais, P. Le; Farcet, Jean Pierre; Wildevuur, Charles; Loisance, D

doi:10.1177/026765919801300605

Cited by 24 publications

(10 citation statements)

References 31 publications

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“…38 Several studies have demonstrated that the release of cytokines, including interleukin-1␤ (IL-1␤), IL-6, IL-8, IL-10, tumor necrosis factor-␣, were significantly reduced with the use of heparincoated circuits. [39][40][41][42][43][44] Reductions in fibrinolysis 45 and in the release of cardiac troponin-I, 46 bactericidal/permeability-increasing protein, and malondialdehyde 48 have also been reported. Lower troponin-I and IL-8 have been linked to reduced myocardial injury in patients undergoing heart or heart-lung transplantation.…”

Section: Effect Of Heparin Coating On Systemic Inflammatory Response In Clinical Bypassmentioning

confidence: 99%

Heparin-coated cardiopulmonary bypass circuits: current status

Hsu

2001

Perfusion

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Heparin-coated circuits have been subjected to vigorous testing, both experimentally and clinically, for the past decade. When the functions of heparin are preserved on the surface, the heparinized surface plays multiple roles in attenuating the systemic inflammatory response. These include the ability to attenuate contact activation, coagulation activation, complement activation and, directly or indirectly, platelet and leukocyte activation. The heparinized surface also renders the cardiopulmonary bypass (CPB) circuits hydrophilic and protein resistant and augments lipoprotein binding. The multifunctional nature of the heparinized surface contributes to the overall biocompatibility of the surface. Clinically, heparin-coated circuits become most effective in reducing systemic inflammatory response and in improving morbidity, mortality, and other patient outcome related parameters when material-independent blood activation is controlled or minimized through a global biocompatibility strategy. Techniques involved in the global biocompatibility strategy are readily available and are being effectively and safely practiced at several centers. With the global biocompatibility strategy, outstanding and reproducible results have been routinely achieved with conventional CPB techniques. Alternative revascularization procedures should equal or surpass conventional CPB, using best clinically proven strategies with respect to patient outcome and long-term graft patency.

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Section: Effect Of Heparin Coating On Systemic Inflammatory Response In Clinical Bypassmentioning

confidence: 99%

Heparin-coated cardiopulmonary bypass circuits: current status

Hsu

2001

Perfusion

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“…Subsequently, the column was flushed 6 times with 1.5 ml of FBS containing the indicated heparin concentration. Fractions (1–7; 1.5 ml each) were then collected and analyzed for the contents of TNF‐α or IL‐6, using commercially available human TNF‐α and IL‐6 immunoassay kits (Endogen Co, Woburn, MA, U.S.A.), respectively.…”

Section: Methodsmentioning

confidence: 99%

“…The technique to immobilize heparin onto the surfaces generally falls into 2 categories, namely, ionically and covalently bonded heparin (4). Several clinical studies have demonstrated that heparin‐coated extracorporeal circuits (5–7) or heparin‐bonded oxygenators (8) reduce the neutrophil and complement activation with an improved clinical outcome and reduced cytokine release. It is known that heparin binds a large number of growth factors and cytokines, including fibroblast growth factors, hepatocyte growth factor, platelet‐derived growth factors, vascular endothelial growth factors, TNF‐α, IL‐1, IL‐2, IL‐6, and IL‐8 (9–14).…”

mentioning

confidence: 99%

Adsorption of Inflammatory Cytokines Using a Heparin‐Coated Extracorporeal Circuit

et al. 2002

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Cardiopulmonary bypass (CPB) surgeries cause an increase in plasma inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) along with whole-body inflammatory responses. The inflammatory responses during a CPB treatment are reduced when using a heparin-coated extracorporeal circuit. Because many cytokines, growth factors, and complements are known to interact with heparin, the reduction of inflammatory responses by a heparin-coated circuit is likely to depend on this heparin-binding nature of the inflammatory cytokines. In this study, the inflammatory cytokines, TNF-alpha and IL-6, in fetal bovine serum (FBS) bound to a heparin-agarose beads (heparin beads)-column and the adsorptions were competitively inhibited on addition of heparin in a concentration-dependent manner. TNF-alpha in FBS required a higher concentration of heparin (50% concentration inhibition [IC50] > 20microg/ml) to inhibit adsorption to the heparin beads-column compared with IL-6, probably because of a stronger interaction between TNF-alpha and heparin-beads. TNF-alpha and IL-6 concentrations in human heparinized blood significantly increased after a CPB treatment. Although the adsorbed amount of IL-6 onto the heparin-coated circuit was low (less than 6% of free circulating IL-6), a significant amount of TNF-alpha adsorbed onto the circuit (23.9-755% of free circulating TNF-alpha). Therefore, the adsorption of inflammatory cytokines, especially TNF-alpha, onto the inner heparin-coated surface of an extracorporeal circuit may partly account for a reduction in inflammatory responses.

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“…The Carmeda circuit appears superior to the Duraflo II in reducing complement, neutrophil activation, and endothelin-1 concentrations. 53,54…”

Section: Strategies To Improve Biocompatibility Of the Extracorporealmentioning

confidence: 99%

Modulation of Systemic Inflammatory Response after Cardiac Surgery

Raja

Dreyfus

2005

Asian Cardiovasc Thorac Ann

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Cardiac surgery and cardiopulmonary bypass initiate a systemic inflammatory response largely determined by blood contact with foreign surfaces and the activation of complement. It is generally accepted that cardiopulmonary bypass initiates a whole-body inflammatory reaction. The magnitude of this inflammatory reaction varies, but the persistence of any degree of inflammation may be considered potentially harmful to the cardiac patient. The development of strategies to control the inflammatory response following cardiac surgery is currently the focus of considerable research efforts. Diverse techniques including maintenance of hemodynamic stability, minimization of exposure to cardiopulmonary bypass circuitry, and pharmacologic and immunomodulatory agents have been examined in clinical studies. This article briefly reviews the current concepts of the systemic inflammatory response following cardiac surgery, and the various therapeutic strategies being used to modulate this response.

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Inflammatory response to cardiopulmonary bypass using two different types of heparin-coated extracorporeal circuits

Cited by 24 publications

References 31 publications

Heparin-coated cardiopulmonary bypass circuits: current status

Heparin-coated cardiopulmonary bypass circuits: current status

Adsorption of Inflammatory Cytokines Using a Heparin‐Coated Extracorporeal Circuit

Modulation of Systemic Inflammatory Response after Cardiac Surgery

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