医学アーカイブ

  • ISSN: 1989-5216
  • ジャーナル h-index: 22
  • 雑誌引用スコア: 4.96
  • ジャーナルのインパクトファクター: 4.44
インデックス付き
  • Genamics JournalSeek
  • 中国国家知識基盤 (CNKI)
  • 研究ジャーナル索引作成ディレクトリ (DRJI)
  • OCLC-WorldCat
  • プロクエスト召喚
  • パブロン
  • ジュネーブ医学教育研究財団
  • ユーロパブ
  • Google スカラー
  • 秘密検索エンジン研究所
このページをシェアする

抽象的な

Remifentanil Attenuates Systemic Inflammatory Response in Patients undergoing Cardiac Surgery with Cardiopulmonary Bypass

Hyun Jung Lee, Tran Duc Tin, Jin Young Kim, Sung Su Chung, Sang Hyun Kwak

Background: Systemic inflammatory response plays pivotal roles in the pathogenesis of organ dysfunction after cardiac surgery with cardiopulmonary bypass (CPB). The aim of this study was to investigate whether remifentanil has the effects on the systemic inflammatory response induced by cardiac surgery with CPB.

Methods: Sixty adult patients undergoing cardiac surgery with CPB were randomly assigned to two groups: a remifentanil (n=30) and a fentanyl group (n=30). The plasma levels of IL-6, IL-8 and malondialdehyde (MDA) were measured at preinduction (T1), just before aortic clamping (T2), just before aortic declamping (T3), 5 (T4), 30 (T5), and 60 (T6) min after aortic declamping. Hemodynamic variables serially recorded at that same times. Myocardial cell damage as assessed by plasma level of creatine kinase-MB (CK-MB) and troponin T were measured before and 24 hours after surgery.

Results: The levels of IL-6, IL-8 and MDA significantly increased from just before aortic declamping in both groups. In the remifentanil group, all of those were significantly lower compared to the fentanyl group from just before aortic declamping (P<0.05). The level of CK-MB and troponin T significantly increased at 24 hours after surgery than preoperative baseline in both groups. In the remifentanil group, both were significantly lower than fentanyl group at 24 hours after surgery.

Conclusion: Remifentanil attenuates systemic inflammatory response more effectively than fentanyl in cardiac surgery with CPB. The mechanism of its effects is likely to be through proinflammatory cytokines (including IL-6, IL-8) and oxidative stress mediator (MDA).