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Adsorption of Inflammatory Cytokines Using a Heparin‐Coated Extracorporeal Circuit
Author(s) -
Fujita Masanori,
Ishihara Masayuki,
Ono Katsuaki,
Hattori Hidemi,
Kurita Akira,
Shimizu Masafumi,
Mitsumaru Atsuhiro,
Segawa Daisuke,
Hinokiyama Kazuhiro,
Kusama Yoshimasa,
Kikuchi Makoto,
Maehara Tadaaki
Publication year - 2002
Publication title -
artificial organs
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.684
H-Index - 76
eISSN - 1525-1594
pISSN - 0160-564X
DOI - 10.1046/j.1525-1594.2002.07017.x
Subject(s) - heparin , cardiopulmonary bypass , extracorporeal , tumor necrosis factor alpha , chemistry , proinflammatory cytokine , extracorporeal circulation , cytokine , pharmacology , inflammation , immunology , medicine , anesthesia , biochemistry
Cardiopulmonary bypass (CPB) surgeries cause an increase in plasma inflammatory cytokines, such as tumor necrosis factor‐α (TNF‐α) 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‐α 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‐α in FBS required a higher concentration of heparin (50% concentration inhibition [IC 50 ] > 20μg/ml) to inhibit adsorption to the heparin beads‐column compared with IL‐6, probably because of a stronger interaction between TNF‐α and heparin‐beads. TNF‐α 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‐α adsorbed onto the circuit (23.9–755% of free circulating TNF‐α). Therefore, the adsorption of inflammatory cytokines, especially TNF‐α, onto the inner heparin‐coated surface of an extracorporeal circuit may partly account for a reduction in inflammatory responses.